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HEABT  DISEASE. 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/heartdiseaseaneuOObrpa 


\ 


Alfred  W.  Sanders,  del. 

Acute  Aortitis    From  recent 

specimen,  showing  raised  pink 

"Gelatmiform    Plaques." 


Geo  Waterston  &  Sous.LiUi,  Edia 


HEART   DISEASE 


AND 


ANEUEYSM  OF   THE  AOETA 

WITH   SPECIAL   REFERENCE   TO 

PROGNOSIS  AND  TREATMENT. 


SIR  WILLIAM  H.  BROADBENT,  Bart.,  K.C.V.O., 

M.D.  Lond.,  F.R.S.,  D.Sc.  Leeds,  LL.D.  Edin.  axd  St.  Andrews,  F.R.C.P., 

PHYSICIAN   IN   OEDINARY  TO   H.JI.    THE   KING,    AND   TO  H.R.H.    THE   PRINCE   OF   WALES  ; 

COMMANDEUR  DE  LA  LEGIO.V  d'HONNETTR  ;  HON'.  MEMBER  OF  VEREIN  FUR  INNERE  MEDICIN,  BERLIN 

AND  OF   GESELLSCHAFT   FUR  INNERE   MEDICIN  UND   KINDEKHEILKUNDE   IN   WIEN, 

AND   OF   SOCIETE   IMPERIALE,    CONSTANTINOPLE; 

VICE-PRESIDENT   IMPERIAL   CANCER   RESEARCH  ;     CHAIRMAN  OF   COUNCIL   OF 

NATIONAL   ASSOCIATION   FOR   PREVENTION  OF   TUBERCULOSIS; 

CONSULTING   PHXSICIAN  TO   ST.   MARY'S   HOSPITAL    AND    TO   THE    LONDON    FEVER   HOSPITAL; 

AND 

JOHN   F.   H.   BROADBENT, 

M.A.,  M.D.  (Oxon.),  F.R.C.P., 

PHYSICIAN  TO   OUT-PATIENTS,    ST.  MARY'S   HOSPITAL;    ASSISTANT   PHYSICIAN  TO   THE 

LONDON  FEVER   HOSPITAL; 

HON.  PHYSICIAN   TO   THE   METROPOLITAN   CONVALESCENT   INSTITUTION; 

FORMERLY   ASSISTANT    PATHOLOGIST   AND   MEDICAL   REGISTRAR  TO  ST.    MARY'S    HOSPITAL. 


FOURTH    EDITION. 


NEW    YORK: 
WILLIAM   WOOD    &  COMPANY. 

MCMVI. 


PREFACE   TO  FOURTH  EDITION. 


My  father,  Sir  William  Broadbent,  has  entrusted  to  rne  the 
preparation  of  the  new  edition  of  this  work,  and  with  his 
approval  I  have  rearranged  the  subject-matter,  and  have 
added  chapters  on  the  pulse,  disease  of  the  coronary  arteries, 
bradycardia,  and  atheroma  of  the  aorta.  I  have  also  revised 
and  rewritten  the  chapters  on  acute  and  malignant  (or  per- 
nicious) endocarditis,  and  that  on  affections  of  the  myocar- 
dium, a  subject  at  which  I  have  been  working  recently. 
I  am  indebted  to  Messrs.  Green  for  permission  to  make 
use  of  the  article  I  wrote  for  the  Encyclopaedia  Medica  on 
affections  of  the  pericardium.  My  father  has  made  several 
important  additions  to  the  chapters  on  angina  pectoris  and 
functional  affections  of  the  heart,  and  has  carefully  revised 
the  whole  of  the  proofs. 

JOHN   F.  H.   BKOADBENT. 

April,  1906. 


PREFACE   TO    THIRD   EDITION. 


Advantage  is  taken  of  the  demand  for  a  new  edition  of 
the  work  on  the  Heart  to  make  the  book  more  complete, 
and  with  this  view  chapters  on  acute  affections  of  the 
heart,  Endocarditis,  Pericarditis,  Myocarditis,  and  on 
Aneurysm  of  the  Arch  of  the  Aorta,  have  been  added. 
In  these,  as  in  the  original  work,  no  attempt  is  made  to 
give  a  systematic  and  complete  treatise  on  each  subject, 
or  to  enter  into  a  discussion  of  conflicting  views  which 
have  been  entertained  on  various  points  of  pathology  and 
etiology.  The  object  has  been  rather  to  endeavour  to 
place  before  the  reader  a  clinical  picture  of  each  disease 
and  to  emphasize  the  points  which  are  of  chief  importance 
in  diagnosis  and  prognosis. 

The  task  of  revision  and  of  making  the  considerable 
additions  which  have  been  specified  has  fallen  almost 
entirely  on  my  son,  Dr.  John  Broadbent,  as  I  myself  have 
not  had  the  requisite  leisure.  The  chapters  on  the  inflam- 
matory affections  of  the  heart  are  entirely  his  work,  and 
the  chapter  on  Aneurysm  has  been  arranged  and  compiled 
by  him  from  notes  and  papers  of  my  own  which  have  been 
published  elsewhere.  While  making  this  acknowledg- 
ment, however,  I  accept  the  responsibility,  as  I  have 
carefully    perused    all   the    new    matter    and   made   some 


viii  PREFACE. 

additions.  Several  illustrations  have  been  added,  for  which, 
with  the  exception  of  Fig.  23,  I  am  indebted  to  Dr.  A.  W. 
Sanders,  whose  coloured  drawing  of  acute  aortitis  from  a 
recent  specimen  is  worthy  of  special  notice. 

W.  H.  BBOADBENT. 

November,  1899. 


PREFACE   TO   FIRST   EDITION, 


This  book  is,  for  the  most  part,  a  reproduction  of  lectures 
on  "  Prognosis  in  Valvular  Disease  of  the  Heart,"  delivered 
before  the  Harveian  Society  in  1884,  and  of  the  Lumleian 
Lectures  at  the  Koyal  College  of  Physicians  on  "  Prognosis 
in  Structural  Diseases  of  the  Heart,"  delivered  in  1891. 

The  prognosis  of  heart  disease  already  engaged  my 
attention  when  I  was  house-physician  under  Sibson  at  St. 
Mary's  Hospital,  and  my  first  paper  on  this  subject  was 
read  before  the  Harveian  Society  in  1866.  Up  to  that 
time  there  had  not,  so  far  as  I  am  aware,  been  any 
systematic  study  and  exposition  of  the  indications  by  which 
the  probable  course  of  disease  of  the  heart  in  different 
cases  might  be  foreseen,  and  ideas  which  tended  to  obscure 
the  interpretation  of  the  symptoms  and  physical  signs  were 
held  by  physicians  of  great  experience  and  authority. 
Traces  of  the  controversies  of  those  days  will  still  be  found 
in  the  present  work.  They  have  lost  much  of  their  interest, 
but  references  to  them  could  not  well  be  entirely  omitted. 

The  prognosis  of  heart  disease  is  worthy  of  special  study, 
not  only  on  account  of  its  inherent  importance,  but  also 
because  the  knowledge  which  enables  the  medical  man  to 
forecast  clearly  the  course  of  the  disease  constitutes  the  best 
preparation  for  its  treatment.     The  subject  of  treatment  did 


x  PREFACE. 

not,  however,  enter  into  the  scheme  of  the  lectures,  but  it 
is  engrafted  upon  them  in  the  present  work,  and  for  this, 
and  for  the  rearrangement  rendered  necessary  by  it,  I  am 
indebted  to  my  son,  Dr.  John  Broadbent,  without  whose 
efficient  assistance  and  co-operation  the  task  of  preparing 
this  book  could  not  have  been  accomplished. 

The  lectures  on  which  the  book  is  based  having  been 
addressed  to  the  College  of  Physicians  and  to  the  Harveian 
Society,  presupposed  a  knowledge  of  heart  disease  on  the 
part  of  my  audience,  and  a  minute  exposition  and  analysis 
of  the  symptoms  and  physical  signs,  by  means  of  which  the 
diagnosis  of  the  different  valvular  and  structural  affections 
of  the  heart  is  arrived  at,  were  therefore  unnecessary.  This 
is  still  taken  for  granted,  but  a  brief  chapter  on  the  exami- 
nation of  the  cardiac  region,  and  on  the  significance  of  the 
various  departures  from  normal  conditions,  has  been  added. 

The  principal  motive  for  reproducing  the  lectures  has 
been  the  frequently  expressed  wish  on  the  part  of  old 
pupils  to  see  my  teachings  on  heart  disease  in  a  collected 
form.  They  have  had  to  wait  long,  and  to  them  I  now 
dedicate  the  book. 

W.   H.  BKOADBENT. 

Sept.  15th,  1897. 


PAGE 


CONTENTS, 


CHAPTER   I. 

The  relations  of  the  heart  to  the  chest  walls — Movements  of  the  heart 
— On  the  methods  of  examination  by  inspection:  palpation,  per- 
cussion, and  auscultation  ... 


CHAPTER   II. 

The  Pulse. 

Methods  of  examining  the  pulse — The  use  of  the  sphygtnograph — 
Arterial  tension— Hypertonus  of  the  vessels — Blood  pressure  and 
instruments  for  estimating  it — Causes  of  high  arterial  tension     ...       17 

CHAPTER   III. 

Diseases  of  the  Pericardium. 

Pericarditis — Morbid  anatomy — Etiology — -Physical  signs — Signs  of 
effusion  and  cardiac  dilatation — Symptoms — -Course  of  the  disease 
— Differential  diagnosis — Prognosis  :  treatment — Adherent  peri- 
cardium— Suppurative  pericarditis — Hydropericardium — Pneumo- 
pericardium, etc ,         29 

CHAPTER  IV. 

Simple  acute  endocarditis     . .         56 

CHAPTER  V. 

"Malignant"  ok  "Pernicious"  Endocarditis. 

Nomenclature  of  the  affection— Morbid  anatomy — Etiology— The  role 
played  by  various  micro-organisms— Physical  signs  and  symptoms 
— Infarction  and  embolism — Diagnosis— Prognosis— Treatment. 
Chronic  endocarditis       67 


CONTENTS. 


CHAPTEE  VI. 

PAGE 

Etiology  of  valvular  lesions 84 


CHAPTEE  VII. 

Valvular  Lesions. 

Points  to  be  considered  in  studying  a  case  of  valvular  disease — The 
physical  signs— Cardiac  murmurs,  their  significance  as  regards  the 
seat  and  as  regards  the  extent  of  the  lesion — Modification  of 
heart-sounds — The  pulse,  its  importance  in  diagnosis        89 

CHAPTEE  VIII. 

The  importance  of  hypertrophy  and  dilatation  of  the  heart  as  a  means 
of  estimating  the  extent  of  a  valvular  lesion — Possible  objections 
to  this  view  discussed — Explanation  of  the  way  in  which  the 
different  valvular  lesions  give  rise  to  hypertrophy  and  dilatation  : 
(1)  Aortic  stenosis ;  (2)  Aortic  incompetence;  (3)  Mitral  regurgi- 
tation;  (4)  Mitral  obstruction — Compensation         100 


CHAPTEE   IX. 

Aortic  Stenosis. 

Morbid  anatomy  and  etiology — The  murmur  of  aortic  stenosis — Con- 
ditions other  than  aortic  stenosis  which  may  give  rise  to  systolic 
aortic  murmurs — Differential  diagnosis  of  murmurs — Estimation  of 
extent  of  lesion  by  means  of  the  murmur,  the  changes  in  the  heart 
and  the  pulse — Progress  of  the  disease  :  Symptoms— Prognosis — 
Treatment  110 


CHAPTEE   X. 

Aortic  Incompetence. 

Etiology — Physical  signs — The  diastolic  murmur  :  directions  in  which 
it  is  conducted — Presystolic  murmur,  its  significance — Modifica- 
tion of  the  aortic  second  sound — Pulsation  of  arteries — Capillary 
pulsation  —  The  collapsing  pulse — -Pulsus  bisfuriens  —  Irregular 
pulse — Estimation  of  the  amount  of  regurgitation  from  the  cha- 
racter of  the  murmur,  of  the  aortic  second  sound,  of  the  pulse,  and 
the  changes  in  the  heart— Aortic  incompetence  due  to  syphilis  and 
causes  other  than  acute  endocarditis — Symptoms— Prognosis — 
Treatment  123 


CONTENTS.  xiii 

CHAPTER   XI. 

Mitral  Incompetence  or  Regurgitation. 

PAGE 

Etiology  and  morbid  anatomy — Physical  signs — The  murmur  of  mitral 
incompetence — The  pulse — Explanation  of  irregularity  of  pulse — 
Mitral  incompetence  due  to  endocarditis — Estimation  of  extent  of 
lesion,  from  character  of  murmur  and  first  sound  and  from  com- 
pensatory changes  in  the  heart — Symptoms — Prognosis — Mitral 
incompetence  without  damage  to  valves — Its  causation  and  ex- 
planation— Differential  diagnosis — Treatment         151 

CHAPTER   XII. 

Mitral  Stenosis. 

Etiology — Predominance  in  the  female  sex— Morbid  anatomy — Physio- 
logy of  the  changes  in  the  heart — Brown  induration  of  lungs — 
Nutmeg  liver — The  physical  sigus — The  pulse — The  changes  in 
the  heart — The  cardiac  murmurs — Three  stages  in  the  progress  of 
the  disease  as  defined  by  auscultatory  signs— The  characteristics 
of  these  three  stages — Symptoms — Diagnosis — Prognosis — Treat- 
ment   174 


CHAPTER  XIII. 

Valvular  Disease  op  the  Right  Side  of  the  Heart. 

Tricuspid    incompetence   and    stenosis — Pulmonic    incompetence  and 

stenosis — Systolic  pulmonic  murmurs  which  do  not  indicate  stenosis     200 

CHAPTER  XIV. 

Congenital  Malformations. 

Varieties  of  congenital  malformations — Relative  frequency  of  occurrence 
— Of  single  and  combined  defects— Physical  signs — Symptoms — 
Cyanosis— Cause  of  cyanosis — Diagnosis — Prognosis  206 

CHAPTER  XV. 

Prognosis  in  Valvular  Disease  (General). 

The  nature  of  the  lesion :  the  relative  danger  attaching  to  each  par- 
ticular lesion — Sudden  death  :  the  valvular  diseases  in  which  it 
is  liable  to  occur— The  extent  of  the  lesion — The  stationary  or 
progressive  character  of  the  lesion  as  influencing  prognosis  ...     214 


CONTENTS. 


CHAPTER  XVI. 

PAGE 

Prognosis  continued — Age,  sex,  heredity —Effects  of  high  arterial 
tension — Habits  and  mode  of  life  of  the  patient— Anaemia — The 
circumstances  under  which  prognosis  may  have  to  be  made :  (1) 
Immediately  after  acute  endocarditis;  (2)  When  the  valvular 
lesion  is  slight  and  has  given  rise  to  no  structural  changes  in  the 
heart ;  (3)  When  compensatory  changes  have  taken  place  but  no 
symptoms  of  embarrassment  of  the  circulation  are  present;  (4) 
When  symptoms  of  failure  of  compensation  have  set  in ;  (5)  In 
advanced  valvular  disease  when  severe  symptoms  of  cardiac  failure 
have  supervened 223 

CHAPTER   XVII. 

Treatment  (General). 

Treatment  of  valvular  disease  in  general — Prophylactic  measures — 
General  rules,  in  cases  where  lesion  is  not  of  serious  extent,  as  to 
exercise,  (Ertel  and  £chott  treatments,  climate,  choice  of  residence, 
diet,  stimulants — Treatment  where  lesion  is  of  more  serious  nature 
and  has  given  rise  to  marked  hypertrophy  and  dilatation  of  the 
heart — Precautions  to  be  taken — Selection  of  winter  resort — Rest 
in  bed — Diet — Stimulants — Employment  of  drugs — Treatment  of 
venous  congestion — Venesection — Treatment  in  aortic  disease      . . .     232 

CHAPTER   XVIII. 

Treatment  by  Drugs. 

Use  and  abuse  of  digitalis — Substitutes  for  digitalis — The  group  of 
cardiac  tonics  of  the  digitalis  type— Their  physiological  action: 
therapeutic  effects — Use  of  digitalis  in  aortic  stenosis,  in  mitral 
incompetence,  in  mitral  stenosis  256 

CHAPTER   XIX. 

Structural  Change  in  the  Heart. 

Hypertrophy — Causes  of  hypertrophy  of  the  left  ventricle,  of  the  right 

ventricle — Physical  signs — Symptoms — Prognosis — Treatment    ...     2G8 

CHAPTER   XX. 

Dilatation. 

Etiology — Valvular  disease,  exertion,  strain,  renal  disease,  acute  bac- 
terial infections — Physical  signs — Symptoms  —Prognosis  —Treat- 
ment   281 


CONTENTS. 

CHAPTEE   XXI. 

Structural  Change  in  the  Eight  Ventricle. 


TAOP, 


Physiological   dilatation — Hypertrophy  and   dilatation — Degeneration 

of  the  muscular  walls      31 1 


CHAPTEE   XXII. 

Disease  of  the  Coronary  Arteries. 

Atheroma   or   Sclerosis  —  Endarteritis  —  Thrombosis  —  Embolism  — 

Aneurysm  ...         ...         ...         ...         ...         ...         •••         ...     320 

CHAPTEE   XXIII. 

Affections  of  the  Myocardium. 

Acute  myocarditis — Fibroid  change — Etiology  and  morbid  anatomy  — 
— Syphilitic  affections  of  the  myocardium — Physical  signs  and 
symptoms  of  fibrosis — Diagnosis — Prognosis — Treatment 32G 

CHAPTEE   XXIV. 

Affections  of  the  Myocardium  (Continued). 

Distinction  between  fatty  infiltration  of  obesity  and  fatty  degeneration 
— Causation  of  fatty  degeneration  —  Symptoms  —  Spontaneous 
rupture  of  the  heart — Physical  signs  —  Diagnosis — Prognosis — 
Treatment — Aneurysm  and  new  growths  of  the  heart         342 

CHAPTEE   XXV. 

Angina  Pectoris. 

Characteristics  of  true  angina — -Associated  symptoms — Exciting  causes 
of  paroxysms  —  Etiology  and  morbid  anatomy — Discussion  of 
theories  advanced  to  explain  the  pain — Diagnosis — Prognosis — 
Treatment  359 

CHAPTEE  XXVI. 

Functional  Affections  (so-called)  of  the  Heart. 

Pain  in  precordial  region— Site  of  pain — Explanation  of  referred  pain 
and  areas  of  cutaneous  hyperalgesia — Disorders  of  rhythm  of  the 
heart — Mechanism  by  which  the  rhythm  of  the  heart  is  regulated 
— Intermittent  and  irregular  action  of  the  heart  —  Palpitation  : 
tachycardia  .,.         ...     381 


CONTENTS. 

CHAPTER  XXVII. 

Disorders  of  Rhythm  of  the  Heart  (Continued). 


TAGE 


Varieties  of  slow  pulse  and  their  causation— The  condition  of  brady- 
cardia known  as  Stokes-Adams  disease — Etiology — Symptoms — 
Diagnosis— Prognosis— Treatment      398 


CHAPTER  XXVIII. 

Acute  Aortitis  or  Acute  Degenerative  Lesions  of  the  Aorta. 

Experimental    evidence — Etiology — Morbid    anatomy — Pathogeny — 

Prognosis — Treatment 405 

CHAPTER  XXIX. 

I  Atheroma  or  Chronic  Degenerative  Lesions  of  the  Aorta. 

Etiology  of  general  arterio-sclerosis  and  atheroma — Morbid  anatomy — 
Pathogeny — Different  views — Physical  signs  and  symptoms— Aortic 
incompetence  due  to  degenerative  change  —  Its  distinguishing 
features — Prognosis — Treatment        411 

CHAPTER  XXX. 

Aneurysm  of  the  Arch  of  the  Aorta. 

Morbid  anatomy — Etiology — Pathogeny — Relations  of  the  arch  of  the 
aorta — Physical  signs  and  symptoms — Aneurysm  (1)  of  the  intra- 
pericardial  portion  of  aorta ;  (2)  of  ascending  aorta ;  (3)  of  trans- 
verse part  of  arch ;  (4)  of  descending  aorta — Diagnosis — Prognosis 
—Treatment        424 

INDEX  475 


HEART   DISEASE. 


CHAPTEE  I. 

THE  EELATIONS  OP  THE  HEAET  TO  THE  CHEST  WALLS — 
MOVEMENTS  OF  THE  HEAET — ON  THE  METHODS  OF  EX- 
AMINATION BY  INSPECTION  :  PALPATION,  PEECUSSION, 
AND    AUSCULTATION. 

A  systematic  description  of  the  anatomy  and  relations  of 
the  heart,  and  a  text-book  exposition  of  the  physical  signs 
by  means  of  which  departures  from  the  normal  condition 
of  the  heart  are  recognized,  would  be  out  of  place  in  a  work 
of  this  character.  A  brief  reminder,  however,  of  the  rela- 
tions of  the  heart  to  the  chest  wall,  together  with  a  short 
description  of  the  method  in  which  a  clinical  examina- 
tion of  the  heart  should  be  conducted,  and  an  indication 
of  the  significance  of  the  various  points  observed,  will 
form  a  useful  preliminary  to  the  study  of  heart  disease. 
This  will  therefore  form  the  subject  of  the  introductory 
chapter. 

The  first  portion  of  this  chapter,  dealing  with  the  position 
and  relations  of  the  heart,  is  mainly  taken  from  the  works 
of  Sibson,*  who  devoted  much  time  and  labour  to  the  study 
of  this  subject,  and  under  whom  I  worked  while  he  was 
engaged  upon  it. 

*  Sibson's  Works,  edited  by  Ord.     Vol.  iii. 

B 


2  heart  disease. 

The  Position  of  the  Heaet  and  the  Eelation  of 
its  Cavities  to  the  Chest  Walls. 

The  heart  and  great  vessels,  with  their  pericardial 
covering,  occupy  the  central  portion  of  the  thoracic  cavity. 
The  right  auricle  and  ventricle  compose  the  whole  of  the 
front  of  the  heart,  with  the  exception  of  a  narrow  strip  to 


FIG.   1. —  RELATION  OF  HEART  TO   CHEST  WALLS  (Sibson). 


the  left,  where  the   left  ventricle   comes   into  view   from 
behind. 

The  right  auricle  lies  behind  the  sternum,  its  upper 
border  being  on  a  level  with  the  third  costal  cartilages,  and 
extending  from  a  point  about  one  inch  to  the  right  of  the 
sternum  nearly  to  its  left  border.  It  is  broadest  above,  and 
narrows  down  almost  to  a  point  at  the  lower  end  of  the 
auriculo-ventricular  furrow,  which  forms  its  left  border  and 
runs  obliquely  downwards  from  the  sternal  end  of  the 
third  left  to  the  sternal  end    of  the  seventh  right   costal 


RELATION  OF  HEART  TO   CHEST  WALLS.  3 

cartilage.  Its  right  border  is  convex,  and  lies  behind  the 
right  costal  cartilages,  just  beyond  the  right  margin  of 
the  sternum. 

The  right  auricle  undergoes  more  change  in  form  during 


X 


y 


p 


p 


FIG.  2. — THE  HEART  AND  GREAT  VESSELS,  WITH  THE  ANTERIOR  WALLS  OF  THE 
RIGHT  AURICLE  AND  RIGHT  VENTRICLE  DISSECTED  OFF  TO  SHOW  POSITION 
OF   THE   VALVES   AND   SEPTA  (QUAIN'S   Anatomy). 

a,  Innominate  and  left  carotid  arteries  ;  b,  Transverse  part  of  arch  ;  c,  Vena  cava  superior  ; 
d.  Ascending  part  of  arch  of  aorta ;  e,  Pulmonary  artery  ;  /,  Pulmonic  valves ;  g,  Appen- 
dix of  left  auricle  ;  h,  Inter-auricular  septum ;  i,  Fossa  ovalis,  with  Eustachian  valve 
below;  j,  Left  segment  of  tricuspid  valve;  Jc,  iDter-ventricular  septum;  I,  Left  ventricle  ; 
m,  Coronary  vein;  n,  Right  segment  of  tricuspid  valve  ;  0,  Inferior  vena  cava  ;  p,  Hepatic 
veins  ;  q,  Left  ventricle  ;  r,  Anterior  papillary  muscle. 

the  action  of  the  heart  than  any  other  portion  of  the  organ, 
becoming  nearly  twice  as  wide  in  systole  of  the  ventricles 
as  in  diastole.     The  auriculo-ventricular  furrow  also  sweeps 


4  HEART  DISEASE. 

backwards  and  forwards  to  so  great  an  extent,  to  the  left 
during  systole  and  to  the  right  during  diastole  of  the 
ventricles,  that  it  presents  no  fixed  position  during  life. 

The  right  ventricle,  when  exposed  to  view,  presents  a 
pyramidal  shape.  The  base  of  the  pyramid  is  formed  by  the 
lower  boundary  of  the  ventricle,  which  rests  on  the  central 
tendon  of  the  diaphragm ;  the  apex  of  the  pyramid  is 
crowned  and  completed  by  the  pulmonary  artery ;  the  left 
side  is  formed  by  the  furrow  which  divides  the  left  from  the 
right  ventricle ;  the  right  side,  by  the  furrow  separating 
the  right  auricle  and  ventricle. 

The  furrow  separating  the  two  ventricles  runs  from  the 
third  to  the  fifth  left  costal  cartilages,  just  behind  their 
junction  with  the  ribs. 

The  left  ventricle  forms  the  convex  left  border  of  the 
heart  as  seen  from  the  front,  and  forms  a  long,  narrow  strip 
extending  from  the  third  left  intercostal  space  down  to  the 
fifth,  where  it  terminates  in  the  apex  of  the  heart.  This 
occupies  the  fifth  space,  being  usually  situated  just  internal 
to  a  line  drawn  vertically  downwards  from  the  nipple. 

The  appendix  of  the  left  auricle  lies  just  behind  the  third 
left  costal  cartilage,  close  to  its  junction  with  the  third  rib, 
and  fills  up  the  space  between  the  upper  end  of  the  left  and 
right  ventricles  at  the  top  of  the  longitudinal  or  inter- 
ventricular furrow. 

The  area  which  would  be  marked  out  on  the  chest 
wall  by  percussion,  indicating  the  position  of  the  heart 
beneath  and  its  relation  to  the  chest  wall,  is  termed  "the 
area  of  deep  cardiac  dulness." 

The  lungs  cover  the  great  vessels  and  the  whole  of  the 
heart  except  a  portion  of  the  right  ventricle. 

The  inner  margins  of  the  right  and  left  lungs  in  front 
meet  behind  the  sternum  for  its  upper  two-thirds.  The 
inner  margin  of  the  left  lung  diverges  from  that  of  the  right 
at  the  level  of  the  fourth  left  costal  cartilage.     It  passes 


RELATION'  OF  HEART    TO    CHEST    WALLS. 


thence  to  the  left  along  the  lower  edge  of  the  fourth 
cartilage  in  front  of  the  body  of  the  right  ventricle,  curving 
downwards  just  before  it  reaches  the  junction  of  the 
cartilage  with  the  rib ;  it  then  crosses  the  fourth  space  and 
fifth  cartilage,  and  curving,  so  as  to  form  a  hollow  space 


FIG.   3. — TUE    HEART    WITH    LUNGS    IN  FIG.  4.— THE   HEART  WITH  OVERLYING 

SITU  TO  ILLUSTRATE  AREA  OF  SUPER-  LUNG  DISSECTED  OFF  TO  ILLUSTRATE 

FICIAL  CARDIAC  DULNESS  (SibsOJl).  AREA   OF   DEEP   DULNESS  (Sibson). 

for   the    lodgment   of   the   apex,    ends    behind    the    sixth 
cartilage. 

The  inner  margin  of  the  right  lung  continues  its  course 
nearly  straight  downwards  behind  and  a  little  to  the  left 
of  the  centre  of  the  sternum,  to  the  level  of  the  sixth 
chondrosternal  articulation.  It  thus  covers  the  right 
auricle,  the  auriculo-ventricular  furrow,  and  the  right  border 
of  the  right  ventricle. 


6  HEART  DISEASE. 

The  area  on  the  chest  wall  corresponding  to  the  part 
of  the  heart  uncovered  by  lung  can  be  accurately  marked 
out  by  percussion,  and  is  known  as  "  the  area  of  superficial 
cardiac  dulness." 

The  area  thus  indicated  would  be  mapped  out  as  follows : 
its  right  margin,  by  a  line  running  from  above  downwards 
slightly  to  the  left  of  the  middle  line  of  the  sternum  from 
the  level  of  the  fourth  costal  cartilage  down  to  that  of  the 
sixth  ;  its  highest  point  would  be  at  the  level  of  the  fourth 
costal  cartilage  ;  its  left  limit  would  be  defined  by  a  line 
running  outwards  from  the  sternum  at  this  level,  along  the 
lower  edge  of  the  fourth  left  costal  cartilage,  nearly  as  far 
as  its  junction  with  the  rib,  and  then  dipping  downwards 
and  curving  slightly  outwards  to  the  point  on  the  chest 
wall  where  the  apex  beat  is  felt.  The  base  or  lower  limit 
corresponds  to  a  line  drawn  from  the  sixth  right  costal 
cartilage  to  the  apex. 

Movements  of  the  Heaet. 

The  heart  undergoes  a  marked  change  in  form  and 
diminution  in  size  during  systole.  At  the  end  of  diastole 
it  is  globular  in  shajDe.  The  apex  is  rounded,  the  ventricles 
are  full,  the  auricles  distended,  the  appendix  of  the  left 
auricle  coming  forward  to  lie  in  the  groove  between  the 
right  ventricle  and  aorta.  The  ventricles  yield  on  handling, 
and  the  auricles  are  dimpled  by  slight  pressure  of  the 
finger.  The  first  systolic  act  is  the  sudden  swift  with- 
drawal of  the  auricular  appendix,  due  to  the  contraction 
of  the  auricle.  Immediately  afterwards  the  ventricles 
harden,  and  the  change  in  form  produced  by  the  contraction 
begins.  The  septum  is  the  centre  on  which  the  movements 
converge,  and  the  most  fixed  point  is  about  three-quarters 
of  the  distance  from  the  apex  to  the  auriculo- ventricular 
furrow.  The  pulmonary  artery  is  drawn  sharply  down- 
wards, the  apex  becomes  more  pointed,  and  moves  spirally 


CLINICAL  EXAMINATION  OF  THE  HEART.  f 

upwards  and  to  the  right.  The  left  border  converges 
slightly,  and  the  right  border  more  upon  the  axis  of  the 
heart. 

The  general  cardiac  impulse  is  due  to  the  contractile 
hardening  of  the  muscular  walls,  the  apex  beat  to  this 
hardening  and  to  the  rotatory  movement  forward  and  to 
the  right.  Both  impulse  and  apex  beat  require  a  fulcrum 
posteriorly  in  order  to  be  felt  through  the  chest  wall. 
This  is  furnished  by  the  pericardium  and  spinal  column, 
against  which  the  shoulder  of  the  left  ventricle  thrusts. 

In  the  interior  of  the  heart  the  end  of  diastole  finds  the 
auriculo-ventricular  valves  floated  up  into  position  by  the 
action  of  elastic  fibres  on  their  auricular  aspect,  and  already 
in  contact  along  their  free  margins,  so  as  to  close  the  orifice. 
The  chordee  tendinese  are  slightly  on  the  stretch.  The 
pressure  on  the  valves  as  the  ventricles  contract  closes 
them  more  tightly,  and  the  co-ordinate  contraction  of  the 
papillary  muscles  neutralizes  the  approximation  of  the 
origin  of  the  chordse  tendinete  to  the  base  of  the  heart 
which  results  from  its  diminution  in  size  during  systole. 
The  contraction  of  the  circular  muscle  fibres  round  the 
orifices  contributes  to  the  complete  closure  of  the  valvular 
flaps. 

The  Clinical  Examination  of  the  Heart. 
This  is  conducted  by  inspection,  palpation,  percussion, 
and  auscultation.  Much  is  learnt  by  careful  inspection. 
Bulging  or  other  general  feature  of  the  precordial  region 
is  to  be  noted.  Any  deformity  of  the  chest  giving  rise  to 
displacement  of  the  heart,  or  fixation  of  one  side  of  the 
thorax  by  pleural  adhesions,  or  by  fibroid  or  other  disease 
of  the  lung,  must  be  taken  into  account.  The  position  and 
character  of  the  apex  beat  should  be  determined  as  far  as 
this  is  possible ;  the  surface  of  the  chest  should  be  care- 
fully scrutinized  for  pulsation  in  abnormal  situations,  and 


8  FIE  ART  DISEASE. 

epigastric  pulsation  or  auy  visible  heave  over  the  right 
ventricle  should  be  noted. 

These  observations  will  be  corroborated  or  checked  by 
palpation  ;  but  there  are  other  points  which  can  be  ascer- 
tained by  the  eye  alone,  such  as  retraction  of  intercostal 
spaces.  This  is  most  commonly  seen  in  the  third,  fourth, 
and  fifth  left  intercostal  spaces  and  is  usually  systolic  in 
time ;  it  may  either  arise  from  a  direct  tug  on  the  spaces 
by  pericardial  adhesions,  or  be  due  to  atmospheric  pressure  : 
the  latter  condition  is  more  common,  and  in  such  cases 
the  heart  will  usually  be  dilated  and  hypertrophied,  and 
therefore  subject  to  great  diminution  in  volume  during 
systole. 

Inspection  also  embraces  the  neck,  where  is  seen  the 
carotid  throb  which  betrays  aortic  regurgitation.  To  be 
characteristic,  it  must  be  visible,  not  at  the  root  of  the 
neck  only,  but  as  high  as  the  hollow  between  the  ramus  of 
the  jaw  and  the  sternomastoid.  It  may,  exceptionally,  be 
present  where  there  is  no  aortic  disease,  and  it  may  be 
simulated  by  pulsation  in  the  deep  jugular  vein.  This, 
however,  is  easily  distinguished,  being  readily  arrested  by 
light  pressure. 

Important  information  may  frequently  be  derived  from 
careful  observation  of  the  veins  of  the  neck.  The  jugulars 
on  one  or  both  sides  may  be  full  and  distended.  If  the  dis- 
tension is  present  on  one  side  only,  it  may  be  due  to  pressure 
on  the  innominate  vein  of  that  side  by  an  aneurysm  or 
some  other  intra-thoracic  tumour.  If  it  exists  on  both  side;-, 
it  may  be  due  either  to  pressure  on  the  superior  vena  cava 
or  both  innominate  veins,  or  to  dilatation  and  engorgement 
of  the  right  side  of  the  heart  from  back  pressure  through 
the  lungs.  In  the  latter  case,  the  veins  will  be  temporarily 
more  or  less  emptied  by  a  forcible  deep  inspiration,  and  will 
become  more  distended  during  expiration  :  in  the  former, 
variations  of  the  intra-thoracic  pressure  during  inspiration 


CLINICAL  EXAMINATION  OF  7 HE  HEART.  9 

and  expiration  will  have  no  appreciable  effect  in  reducing 
or  augmenting  the  distension.  Pulsation  of  the  jugular 
veins  may  be  present  when  the  right  side  of  the  heart  is 
greatly  dilated  and  tricuspid  regurgitation  has  set  in.  The 
pulsation  is  often  double,  both  auricular  and  ventricular 
systoles  transmitting  backward  waves.  It  has  been  studied 
with  great  care  by  Mackenzie,  of  Burnley,  who  has  obtained 
graphic  records  of  two  distinct  types  of  jugular  pulsation, 
and  established  their  significance. 

Finally,  mention  may  be  made  of  enlarged  and  tortuous 
veins  on  the  surface  of  the  chest,  constituting  collateral 
channels  between  the  superior  and  inferior  vense  cavse  when 
one  or  other  is  compressed,  and  of  pulsating  veins  occasion- 
ally seen  dipping  into  an  intercostal  space  near  the  sternum. 

Palpation. — The  information  obtained  by  palpation  is 
second  in  importance  only  to  that  afforded  by  auscultation. 
The  situation,  force,  limits,  and  extent  of  the  cardiac  im- 
pulse are  accurately  ascertained,  and  the  relative  intensity 
of  the  apex  beat  and  right  ventricle  beat  must  be  compared. 
The  examination,  to  be  complete,  must  be  conducted  in 
various  ways. 

Firstly,  the  flat  of  the  right  hand  should  be  placed  over 
the  cardiac  area,  the  fingers  covering  the  apex  region.  The 
powerful  heaving  impulse  of  the  apex  in  hypertrophy,  the 
diffuse  shock  or  slap  in  dilatation,  and  the  peculiar  sudden 
tap  in  mitral  stenosis  are  often  at  once  diagnostic :  a  power- 
ful heave  of  the  lower  left  costal  cartilages,  and  sometimes 
of  the  lower  end  of  the  sternum  as  well,  will  indicate  stress 
thrown  on  the  right  ventricle  by  back  pressure  through  the 
pulmonary  circulation.  Thrills  or  vibrations,  systolic  or  pre- 
systolic, over  the  area  of  the  apex  beat  or  elsewhere  will  be 
recognized  at  the  same  time.  Sometimes  a  peculiar  diastolic 
shock  or  retraction  may  be  felt  over  the  apex  or  the  right 
ventricle,  caused  by  the  presence  of  pericardial  adhesions. 
Next  the  fingers  must  be  pressed  into  the  right  intercostal 


io  HEART  DISEASE. 

spaces  in  search  of  pulsation,  and  the  apex  region  must  be 
explored  with  the  tips  of  the  fingers,  and  the  exact  position, 
extent,  force,  and  deliberate  or  sudden  character  of  the  apex 
beat  must  be  noted.  This  investigation  must  not  be  limited 
to  the  point  at  which  the  apex  appeared  to  present  itself, 
when  the  hand  was  applied  to  the  praecordium ;  the  real 
apex  beat  may  be  sometimes  far  out  in  the  axilla,  or  high 
up  in  the  fourth  space,  or  it  may  be  concealed  behind  the 
mamma. 

(Speaking  generally,  displacement  of  the  apex  downwards 
is  indicative  of  hyjDertrophy  of  the  left  ventricle,  dilatation 
giving  rise  to  extension  of  the  impulse  outwards  and  down- 
wards ;  displacement  of  the  apex  to  the  left  is  caused  by 
enlargement  of  the  right  ventricle,  which  is  usually  due  to 
combined  hypertrophy  and  dilatation.  For  the  most  part, 
any  considerable  change  in  the  position  of  the  apex  beat 
is  the  result  of  hypertrophy  and  dilatation  of  both  sides 
of  the  heart.  Special  displacement  of  the  apex  not  due 
to  intrinsic  changes  in  the  heart  may  be  the  result  of 
various  causes,  such  as  pericardial  or  pleuro-pericardial 
adhesions,  pleural  effusion,  pneumo-thorax,  fibroid  condition 
or  cavitation  of  the  lung,  or  deformity  of  the  chest.  It 
is  always  well  to  ascertain  whether  the  aj)ex  changes  its 
position  in  respiration,  and  with  change  of  posture  of  the 
patient  from  the  erect  to  the  recumbent  position,  and  when 
lying  first  on  one  side,  then  on  the  other. 

It  is  not  uncommon  to  find  that  neither  apex  beat  nor 
impulse  of  any  kind  is  to  be  felt.  This  does  not  necessarily 
imply  feeble  action  of  the  heart,  but  may  be  due  to 
thickness  of  the  parietes  or  great  depth  of  thorax,  or  to 
overlapping  emphysematous  lung,  or  to  pericardial  adhesions. 

Departures  from  the  normal  in  the  cardiac  rhythm  should 
also  be  noted ;  they  are  of  two  kinds :  Irregularity  and 
Intermission — irregularity,  when  the  beats  are  of  varying 
force  and  follow  each  other  at  unequal  intervals;  intermission, 


CLINICAL  EXAMINATION  OF  THE  HEART.  n 

when  a  beat  is  dropped  from  time  to  time,  the  intervening 
beats  being  of  equal  force  and  at  equal  intervals. 

The  irregular  action  of  the  heart  is  usually  exaggerated 
in  the  pulse,  as  many  of  the  beats  may  fail  to  reach  the 
wrist.  When  the  pulse  is  intermittent,  it  will  usually  be 
found  that  there  is  not  an  entire  absence  of  the  beat  of  the 
heart,  but  an  imperfect  and  hurried  beat  corresponding  to 
the  intermission. 

The  examination  by  palpation,  to  be  complete,  must 
embrace  the  abdomen,  and  the  size  of  the  liver  must  be 
carefully  ascertained.  As  the  right  ventricle  begins  to  fail, 
and  obstruction  to  the  return  of  blood  to  the  heart  from 
the  liver  through  the  inferior  vena  cava  begins  to  be  felt, 
the  liver  becomes  engorged  and  congested,  and  gradually 
increases  in  size,  till  it  may  become  very  much  enlarged, 
extending  even  below  the  umbilicus.  The  size  of  the  liver 
is  therefore  an  important  index  as  to  the  degree  of  venous 
obstruction. 

In  examining  to  ascertain  the  size  of  the  liver,  the 
patient  should  be  made  to  lie  on  his  back  with  the  legs 
drawn  up,  so  that  the  belly  is  perfectly  flaccid.  The  flat 
of  the  hand  should  then  be  placed  on  the  abdomen,  and  the 
edge  of  the  liver  carefully  felt  for ;  at  the  same  time  the 
other  hand  should  be  placed  beneath  the  back  of  the  patient 
below  the  false  ribs,  and  the  liver  lifted  from  behind,  so 
that  if  the  liver  edge  is  not  at  first  felt,  the  jogging  from 
behind  will  press  it  up  against  the  hand  on  the  abdomen, 
and  render  it  more  obvious.  Palpation  with  the  tips  of  the 
fingers  will  probably  provoke  some  rigidity  of  the  abdominal 
walls,  which  obscures  the  resistance  presented  by  the  liver 
behind.  When,  however,  there  is  fluid  present  in  the 
abdominal  cavity,  this  method  of  palpation  will  be  useful, 
for  then  on  dipping  sharply  down  with  the  fingers,  the 
fluid  between  the  liver  and  abdominal  walls  will  be  dis- 
placed, and  the  firm,  hard  substance  of  the  liver  be  felt  below. 


12  HEART  DISEASE. 

Percussion  is,  as  a  rule,  a  very  untrustworthy  method 
of  ascertaining  the  size  of  the  liver,  owing  to  conducted 
resonance  from  distended  coils  of  intestine  ;  it  will,  however, 
serve  to  mark  out  the  upper  margin  of  the  liver,  unless  there 
he  consolidation  of  lung  fluid  or  old  pleural  adhesions  at 
the  base  of  the  right  pleural  cavity. 

Pulsation  of  liver  is  best  detected  by  combined  simul- 
taneous palpation  and  inspection.  The  hand  should  be 
placed  on  a  part  of  the  liver  at  some  distance  from  the 
epigastrium,  and  gentle  pressure  being  made,  it  should  be 
carefully  watched.  If  the  liver  is  actually  pulsating,  and 
not  merely  jogged  by  a  hypertrophied  right  ventricle,  the 
hand  will  be  seen  to  rise  and  fall  rhythmically  even  though 
no  actual  pulsation  is  felt  on  palpation. 

Percussion. — Percussion  will  verify  and  perhaps  extend 
the  information  obtained  by  inspection  and  palpation.  It 
is  specially  useful  when  no  impulse  is  present.  There  is 
normally,  as  has  already  been  described,  a  small  area  of 
absolute  dulness — "  the  superficial  cardiac  dulness  " — where 
the  heart  is  not  covered  by  lung,  which  is  easily  defined. 
It  may  be  encroached  upon  and  obliterated  when  the  lungs 
are  emphysematous,  or  extended  when  they  are  shrunken 
as  a  result  of  fibroid  contraction  or  pleural  adhesion.  The 
deep  dulness  indicating  the  true  dimensions  of  the  heart 
cannot  be  mapped  out  with  absolute  accuracy  in  all  cases, 
as  the  overlying  lung  tissue  varies  in  thickness  and  extent 
in  different  individuals,  and  in  inspiration  and  expiration. 
In  percussing  for  this  purpose,  the  finger  must  be  pressed 
firmly  into  the  intercostal  spaces,  and  the  stroke  must  be 
delivered  smartly  and  perpendicularly.  The  note  changes 
gradually  as  the  dull  area  is  left  with  the  increase  in  the 
thickness  of  the  overlapping  lung,  till  full  lung  resonance 
is  reached.  The  end  of  expiration,  when  the  cushion  of 
lung  is  thinnest,  should  be  chosen  as  the  moment  to  attempt 
the  definition  of  the  comparative  dulness  which  indicates 


CLINICAL  EXAMINATION  OF  THE  HEART.  13 

the  size  and  position  of  the  heart.  The  so-called  auscul- 
tatory percussion  is,  in  my  opinion,  of  no  value  whatever. 

Auscultation. — The  physical  examination  is  completed 
by  auscultation.  For  the  most  part,  a  diagnosis  has  already 
been  arrived  at  before  the  stethoscope  is  applied,  and  in 
all  cases  the  information  obtained  by  auscultation  must  be 
checked  and  interpreted  by  evidence  derived  from  the  pulse, 
and  from  inspection,  palpation,  and  percussion.  Either  a 
flexible  or  rigid  stethoscope  may  be  employed.  The  former 
is  more  convenient  and  expeditious,  as  it  can  be  shifted 
from  point  to  point  without  moving  the  head,  and  it  is 
always  under  the  eye,  so  that  bulging  or  retraction  of  spaces 
can  be  timed  and  co-ordinated  with  the  sounds  or  murmurs 
heard.  On  the  other  hand,  it  is  sometimes  difficult  to  dis- 
tinguish between  the  first  and  second  sound,  and  the  rigid 
stethoscope,  by  communicating  a  faint  jar  to  the  ear,  at 
once  points  out  the  sound  which  is  produced  by  the  systole. 

The  stethoscope  should  be  applied  successively  to  the 
apex  region,  the  tricuspid,  pulmonic,  and  aortic  areas,  and 
the  character,  and  absolute  and  relative  loudness  of  the 
sounds  should  be  noted  at  each  point ;  observations  taken 
simply  at  the  apex  or  base  afford  very  imperfect  information. 

The  Mitral  Area. — At  the  apex  both  sounds  are  normally 
audible — the  first,  comparatively  long  and  low-pitched ;  the 
second,  short  and  sharp.  The  first  sound  may  undergo 
various  modifications.  It  may  be  prolonged,  which  is 
usually  indicative  of  hypertrophy;  or,  on  the  other  hand, 
it  may  be  short  and  sharp.  If  when  short  it  is  also  loud, 
it  is  among  the  indications  of  dilatation  ;  if  weak,  it  may 
be  due  either  to  degeneration  or  to  simple  asthenia  of  the 
cardiac  muscle.  A  peculiar  sharp  and  snapping  character 
of  the  first  sound  at  the  apex  is  produced  by  mitral 
stenosis.  Reduplication  of  the  first  sound  is  an  important 
modification  often  met  with ;  it  is  most  distinct  when  the 
stethoscope  is  placed  exactly  over  the  septum  between  the 


14  HEART  DISEASE. 

apex  and  right  ventricle,  i.e.  partly  over  one  ventricle, 
partly  over  the  other.  Left  of  this  spot  the  sound  may  be 
merely  blurred;  right  of  it,  reduplication  may  still  be 
distinct.  The  double  sound  is  due  to  want  of  synchronism 
between  the  two  ventricles,  and  may  be  produced  when- 
ever undue  stress  is  put  upon  the  left  ventricle  by  high 
systemic  arterial  tension,  or  on  the  right  by  obstruction  in 
the  pulmonary  circulation.  The  second  sound  heard  at 
the  apex  is,  for  the  most  part,  that  produced  at  the  aortic 
valves ;  occasionally  it  is  more  distinct  here  than  at  the 
aortic  area  proper.  Its  modifications  will  be  described 
when  the  sounds  at  the  base  are  discussed. 

The  interval  between  the  first  and  second  sounds  indi- 
cating the  duration  of  the  cardiac  systole,  and  that  between 
the  second  and  first  sounds,  or  the  diastolic  interval, 
should  be  carefully  observed,  and  any  deviation  from  the 
normal  noted.  The  rhythm  may  be  disturbed  in  one 
direction  by  the  shortening  of  the  diastolic  interval,  till 
the  sounds  are  equidistant  and  resemble  the  ticking  of  a 
watch,  as  in  palpitation,  or  the  sounds  may  become  equi- 
distant from  prolongation  of  the  systole,  when  they  resemble 
the  beat  of  a  pendulum.  In  the  other  direction  the  systolic 
interval  may  be  shortened  till  the  second  sound  follows 
the  first  almost  without  an  appreciable  pause  :  this  is  a 
serious  condition,  indicating  incomplete  contraction  of  the 
ventricle,  and  also,  in  many  cases,  impending  cardiac 
failure. 

The  murmurs  heard  at  the  apex  may  be  systolic,  pre- 
systolic, or  diastolic;  of  these  the  most  frequent  is  the 
systolic.  It  is  most  commonly  smooth  and  blowing  in 
character  ;  sometimes  a  musical  element  may  be  present,  or 
the  murmur  may  be  rumbling  and  indistinct ;  it  is  rarely 
rough  and  croaking,  as  is  often  the  case  with  aortic  systolic 
murmurs.  The  systolic  murmur  heard  at  the  apex  always 
signifies    more   or   less  regurgitation   through    the   mitral 


CLINICAL  EXAMINATION  OF  THE  HEART.  15 

orifice,  and  it  will  be  necessary  to  note  how  far  outside  the 
apex  the  murmur  is  audible,  and  to  what  extent  it  replaces 
the  first  sound,  as  these  will  be  important  points  in  esti- 
mating its  significance.  An  apex  murmur  is  sometimes 
more  distinct  in  the  recumbent  than  in  the  sitting  or  erect 
position,  or  may  be  brought  out  by  slight  exertion. 

A  pulmonic  or  aortic  systolic  murmur  may  be  conducted 
to  the  apex,  but  it  will  be  of  diminished  intensity  and  will 
not,  as  a  rule,  be  conducted  towards  the  axilla. 

The  presystolic  murmur,  so  named  from  the  fact  that  it 
precedes  and  runs  up  to  the  first  sound  produced  by  the 
cardiac  systole,  is  usually  vibratory  in  character.  Speaking 
generally,  it  indicates  the  presence  of  mitral  stenosis,  and 
is  produced  by  the  rush  of  blood  from  the  auricle  into  the 
ventricle  through  the  narrowed  mitral  orifice  ;  but  it  may  be 
present  as  a  temporary  phenomenon  after  acute  disease. 
In  an  early  stage  it  is  brief  in  duration,  and  rises  rapidly 
in  intensity,  terminating  abruptly  in  the  first  sound,  when 
it  corresponds  with  and  is  produced  by  the  auricular  systole. 
It  may,  however,  be  greatly  prolonged ;  that  is,  it  may  begin 
at  a  much  earlier  period  so  as  to  correspond  with  the  active 
dilatation  stage  of  the  ventricular  diastole,  which  precedes 
the  auricular  systole. 

A  diastolic  murmur  audible  at  the  apex  is  usually  that 
of  aortic  insufficiency,  conducted  from  the  base  to  the  apex 
by  the  walls  of  the  heart. 

The  Tricuspid  Area. — The  sounds  heard  over  the  tri- 
cuspid area  are  mainly  those  of  the  right  ventricle;  the 
first  sound  is  rather  shorter  and  louder  than  that  at  the 
apex,  and  the  second  sound  is  intensified  when  there  is 
obstruction  in  the  pulmonary  circulation. 

Systolic,  presystolic,  and  diastolic  murmurs  may  be 
heard  in  this  region,  and  the  former  may  indicate  tricuspid 
incompetence,  but  the  two  latter  varieties  are  most  com- 
monly murmurs  conducted  from  the  apex  or  base,  and 
cannot  be  relied  upon  for  diagnostic  purposes. 


16  HEART  DISEASE. 

The  Aortic  Area. — In  the  pulmonic  and  aortic  areas 
accentuation  of  the  second  sound  is  the  point  specially  to 
be  observed,  denoting  increased  pressure  in  the  pulmonic 
or  systemic  circulation  respectively.  Keduplication  of  the 
second  sound  is  not  uncommon,  and  is  due  to  a  synchronous 
closure  of  the  aortic  and  pulmonic  semilunar  valves. 

The  murmurs  audible  over  the  aortic  area  in  the  second 
right  intercostal  space  may  be  systolic  or  diastolic.  A 
systolic  murmur  may  indicate  actual  obstruction,  but  is 
more  frequently  due  to  mere  roughening  or  rigidity  of  the 
cusps  of  the  valves,  or  to  dilatation  of  the  aorta  beyond  the 
valves,  or  other  conditions  not  necessarily  causing  narrow- 
ing of  the  orifice.  It  may  be  loud  and  rough,  or  musical, 
or  soft  blowing.  A  diastolic  murmur  is  usually  blowing  in 
character,  and  almost  invariably  indicates  aortic  incom- 
petence, being  produced  by  the  regurgitant  stream  of  blood ; 
it  can  sometimes  be  heard  lower  down  over  the  sternum, 
or  a  little  to  one  side  of  it,  at  a  point  nearer  the  orifice 
of  the  aorta,  when  it  is  not  audible  in  the  so-called  aortic 
area. 

The  Pulmonic  Area. — Systolic  and  diastolic  murmurs 
may  also  be  heard  in  the  pulmonic  area,  the  third  left 
intercostal  space,  and  may  indicate  stenosis  or  incompetence 
of  the  pulmonic  valves.  These  affections  are,  however, 
rare,  and  are  usually  of  congenital  origin.  The  murmurs 
heard  in  the  pulmonic  region  are  for  the  most  part  either 
conducted  from  the  region  of  the  aorta  or  apex,  or  are 
hseinic  murmurs  dependent  on  abnormal  conditions  of  the 
blood,  or  they  may  occasionally  be  due  to  vibrations  caused 
by  the  contact  of  the  conus  arteriosus  with  the  chest  wall. 
A  diastolic  aortic  murmur  is  frequently  louder  in  the  pul- 
monic area  than  at  the  right  second  space,  and  may  be 
audible  here  when  it  cannot  be  heard  in  the  aortic  area. 


CHAPTER   II. 
THE    PULSE. 

METHODS  OF  EXAMINING  THE  PULSE —THE  USE  OP  THE 
SPHYGMOGRAPH — ARTERIAL  TENSION — HYPERTONUS  OF 
THE  VESSELS — BLOOD  PRESSURE  AND  INSTRUMENTS 
FOR  ESTIMATING  IT  —  CAUSES  OF  HIGH  ARTERIAL 
TENSION. 

A  careful  and  systematic  examination  of  the  pulse  is  of 
the  first  importance,  inasmuch  as  the  heart  and  arteries 
together  constitute  one  system,  and  are  in  close  mechanical 
and  functional  relation. 

In  feeling  the  pulse,  three  fingers  should  be  placed  on 
the  vessel,  and  careful  palpation  be  made  with  varying 
degrees  of  pressure.  The  following  points  should  be  care- 
fully noted  : — 

1.  The    frequency,  that  is,   the    number   of  beats   per 

minute  ;  the  regularity  or  irregularity  of  the  beats, 
and  their  equality  or  inequality  in  force. 

2.  The  size  of  the  vessel,  whether  large  or  small. 

3.  The    character     of    the     beat,    whether   abrupt     or 

gradual,  long-sustained   or  short,    subsiding   gra- 
dually or  falling  abruptly. 

4.  The  force  or  strength  of  each  beat. 

5.  The  condition  of  the  vessel  between  the  beats,  whether 

full  and  resistant  or  readily  compressible. 

6.  The    state    of    the    arterial    wall,    whether    smooth, 

regular,  and  supple,  or  irregular,  tortuous,  and  rigid. 

c 


1 8  HEART  DISEASE, 

The  determination  of  the  frequency,  the  regularity  or 
irregularity  of  the  pulse,  the  size  of  the  vessel,  the  character 
of  the  beat,  presents  little  difficulty. 

To  estimate  the  force  of  each  beat,  three  fingers  should 
be  placed  on  the  vessel,  and  pressure  made  by  the  finger 
nearest  the  heart  till  the  wave  is  arrested,  so  that  it  is  not 
felt  by  the  two  lower  fingers.  By  varying  the  degree  of 
pressure  with  one  and  all  three  fingers,  some  idea  is  formed 
of  the  force  of  the  pulse  wave. 

It  must  be  recollected  that  the  radial  artery  when 
compressed  by  the  finger  is  more  or  less  flattened.  When 
distended  by  the  increased  pressure  from  the  volume  of 
blood  injected  into  the  arterial  system  at  each  beat  of  the 
heart  it  tends  to  resume  the  circular  shape,  and  this  is  felt 
by  the  finger  as  the  pulse  wave.  It  yields  gradually  as 
the  pressure  within  subsides,  and  in  the  normal  sphygmo- 
graphic  tracing  the  cycle  is  represented  graphically  by  a 
sudden  sharp  systolic  rise,  followed  by  a  gradual  fall, 
which  is  interrupted  by  a  slight  secondary  elevation  due  to 
the  dicrotic  wave. 

Condition  of  the  Artery  between  the  Beats. — The  artery  is 
more  or  less  distended  with  blood  between  the  beats  after 
the  wave  has  passed,  and  the  degree  of  pressure  within 
the  vessel  during  that  period  may  be  termed  the  constant 
mean  blood  pressure.  It  is  also  known  as  the  "  diastolic 
pressure,"  but  the  term  is  misleading,  as  the  pressure  is 
maintained  by  the  elastic  recoil  of  the  aorta  and  large 
vessels,  and  has  no  reference  to  the  heart.  The  term 
"  systolic  pressure  "  is  more  justifiably  employed  to  denote 
the  increased  or  variable  pressure  due  to  the  blood  in- 
jected at  each  beat  of  the  heart.  If  the  arterial  walls 
are  relaxed  and  the  blood  pressure  is  low,  the  vessel  can 
readily  be  flattened,  and  can  scarcely  be  felt  by  the 
finger  between  the  beats.  The  filling  of  the  artery  at  each 
systole  of  the  heart  will  then  make  a  greater  impression  on 


THE  PULSE.  19 

the  finger,  and  will  jerk  up  the  lever  of  the  sphygraograph 
more  rapidly  and  to  a  greater  height,  while  the  fall  will  be 
more  abrupt  and  the  dicrotic  rebound  well  marked. 


FIG.    5. — LOW-TENSION   PULSE,   SHOWING   DICROTISM. 


-FIG.    6. — HIGH-TENSION   PULSE. 

When  the  artery  is  contracted  and  in  a  condition  of 
hypertonus  (to  which  reference  will  be  made  later),  and  the 
blood  pressure  is  high,  the  vessel  is  not  easily  flattened  by 
the  finger  or  lever  of  the  sphygmograph.  The  wave 
appears  to  be  small  and  the  excursion  of  the  lever  is 
limited,  so  that  the  pulse  may  appear  to  be  weak,  until 
more  pressure  is  made,  when  its  true  character  will  be 
brought  out,  and  the  greater  the  pressure  made  the  stronger 
the  pulse  will  appear  to  be.  The  tracing  will  have  a  less 
abrupt  upstroke,  and  will  be  of  no  great  height,  while  the 
summit  may  be  rounded,  and  the  descent  gradual,  and 
unbroken  by  a  dicrotic  wave.  By  the  fingers  the  artery 
will  be  felt  as  a  firm  rounded  cord,  and  will  not  be  easily 
compressed. 

It  is  important,  therefore,  to  carefully  examine  the 
artery  between  the  beats,  rolling  it  beneath  the  fingers  and 


20  HEART  DISEASE. 

making  varying  degrees  of  pressure,  so  as  to  form  an  esti- 
mate of  the  mean  or  constant  blood  pressure — in  other  words, 
of  the  "  arterial  tension." 

The  condition  of  the  arterial  walls  should  also  be 
noted,  as  to  whether  they  are  soft  and  flexible,  thickened 
from  hypertrophy,  or  rigid,  tortuous,  and  deformed  from 
degenerative  changes.  For  this  purpose  the  blood  is 
pressed  out  of  the  vessel,  which  is  then  rolled  under  the 
fingers  and  carefully  palpated  by  carrying  them  along  it, 
so  that  rigidity  or  inequalities  in  its  course  may  be  detected. 

Most  of  these  points,  such  as  the  force  and  frequency 
and  height  of  the  pulse  wave,  the  size  of  the  vessel,  its  ful- 
ness or  collapse  between  the  beats,  and  thickening  of  its 
walls,  can  readily  be  determined  by  the  fingers  of  the 
practised  observer. 

A  sphygmographic  tracing  will  form  a  useful  supple- 
mentary graphic  record  of  the  character  of  the  pulse  wave, 
and  will  be  the  most  trustworthy  criterion  as  to  its  height 
and  duration,  a^  to  whether  its  rise  and  subsidence  are 
gradual  or  abrupt,  and  as  to  the  presence  or  absence  of 
dicrotism,  etc.  A  comparison  of  a  sphygmographic  tracing 
from  the  radials  of  both  sides  will  indicate  whether  the  two 
pulses  differ  in  character,  and  will  often  be  of  great  value 
as  an  aid  to  the  diagnosis  of  aneurysm.  Marey's  sphygmo- 
graph  is  the  most  trustworthy  instrument,  as  the  instru- 
mental oscillations  in  Dudgeon's  sphygmograph  often 
vitiate  results,  especially  when  the  rise  of  the  wave  is 
sudden  and  violent  and  its  fall  abrupt. 

Arterial  Tension. — There  is,  however,  one  important  point 
as  to  which  confusion  is  liable  to  arise.  This  is  the  question 
as  to  the  meaning  of  the  term  "  arterial  tension."  As  this 
has  an  important  bearing  on  prognosis,  and  reference  will 
be  frequently  made  to  it  in  this  volume,  it  may  be  as  well 
to  discuss  the  subject  fully  now.  By  "  arterial  tension  " 
is   here   meant   the   strain  to  which   the   arterial    wall   is 


ARTERIAL    TENSION.  21 

subjected  by  the  contained  blood  between  the  beats  of  the 
heart — in  other  words,  it  is  a  measure  of  the  constant  mean 
blood  pressure,  as  expressed  by  the  strain  it  exerts  on  the 
arterial  walls. 

The  factors  which  enter  into  its  production  are,  first  and 
foremost,  the  peripheral  resistance  in  the  capillaries  and 
arterioles  ;  secondly,  the  volume  of  blood  thrown  into  the 
aorta  at  each  systole  of  the  heart ;  thirdly,  the  force  of  the 
heart  beat. 

To  take  a  simple  illustration,  if  we  have  a  fire-hose  with 
a  powerful  pump  at  one  end  and  a  narrow  nozzle  at  the 
other,  the  hose-pipe  will  remain  full  and  distended  between 
each  stroke  of  the  pump,  and  the  mean  tension  maintained 
will  be  very  high.  If  we  remove  the  nozzle,  whatever  be 
the  force  of  each  stroke  of  the  pump  and  the  quantity  of 
water  injected,  the  mean  constant  tension  will  be  practically 
nil,  or  very  low,  and  the  hose-pipe  will  be  flaccid  between 
each  stroke  of  the  pump.  By  increasing  the  force  of  the 
pump  and  the  volume  of  water  injected,  the  momentary 
strain  on  the  walls  of  the  hose  at  each  stroke  will  be 
greater,  but  the  constant  mean  tension  will  still  be  very 
low  if  there  is  no  nozzle  at  the  distal  end. 

The  heart  corresponds  to  the  pump,  the  arterial  tree 
to  the  hose-pipe,  and  the  peripheral  resistance  afforded  by 
the  arterioles  and  capillaries  to  that  generated  by  the 
narrow  nozzle  at  the  distal  end  of  the  hose-pipe.  It  is 
true  that  the  analogy  does  not  hold  good  in  all  points,  for 
in  the  hose-pipe  we  have  an  inelastic,  more  or  less  rigid, 
tube,  whereas  the  arterial  system  is  composed  of  a  series  of 
elastic  contractile  vessels  ;  moreover,  the  aorta  constitutes 
an  elastic  reservoir,  which  tends  to  make  the  flow  of  blood 
less  jerky  and  more  continuous,  the  pressure  more  constant, 
and  the  strain  less  severe,  in  the  arteries  of  less  size.  I 
have  thought  it  worth  while  to  give  this  simple  illustration, 
as   the    statement   is  made   by   Professor   Clifford  Allbutt 


22  HEART  DISEASE. 

"  That  in  aortic  regurgitation  the  mean  arterial  tension 
is  higher  than  in  any  other  disease."  *  And  again,  "  The  in- 
comprehensible statement  is  commonly  repeated  that  in 
aortic  regurgitation  the  tension  is  low."  f 

If  we  apply  our  illustration  to  aortic  regurgitation  (ex- 
cluding that  due  to  strain  or  degenerative  changes),  we  shall 
see  that  it  is  impossible  for  the  mean  arterial  tension  to  be 
high. 

For  though  in  aortic  regurgitation  we  have  a  more 
powerful  pump  than  normal  from  the  hypertrophy  of  the 
heart,  and  a  greater  volume  of  blood  injected  into  the 
arterial  sj^stem  at  each  beat,  from  the  increased  capacity  of 
the  dilated  left  ventricle,  and  the  initial  momentary  strain 
on  the  vessel  walls  during  systole  is  severe,  yet  immedi- 
ately after  the  systole  blood  leaks  back  into  the  heart ;  the 
vessel  walls  are  consequently  not  kept  on  the  stretch  by  the 
contained  fluid,  but  tend  to  collapse,  so  that  the  mean  con- 
stant tension  between  each  heart-beat  will  necessarily  be 
low,  in  proportion  as  the  regurgitation  is  considerable. 
Clifford  Allbutt,  in  his  article,  obviously  does  not  use  the 
term  "  arterial  tension  "  in  the  same  sense  as  it  is  employed 
here,  but  rather  as  a  synonym  for  the  initial  distensile 
strain  at  the  moment  of  the  cardiac  systole. 

The  mean  constant  tension  or  strain  on  the  arterial 
walls  can  be  most  accurately  estimated  by  determining  the 
blood  pressure  in  each  instance,  and  if  in  man  we  could,  as 
in  animals,  connect  the  column  of  blood  within  an  artery 
with  a  manometer  by  means  of  a  rigid  tube,  this  would 
afford  a  trustworthy  criterion. 

Obviously  this  method  is  impracticable  in  dealing  with 
man,  and  various  instruments  have  been  devised  in  its 
place,  the  essential  principle  of  which  is  an  attempt  to 
balance   the  pressure  of  the    blood    within   an   artery   by 

*  "System   of  Medicine,"  vol.  v.  p.   937,  line  32;   article   on  "Aortic 
Regurgitation." 
t  Ibid.,  p.  93G. 


BLOOD  PRESSURE.  23 

graduated  pressure  applied  externally  to  its  walls.  The 
degree  of  pressure  required  to  arrest  trie  flow  of  blood 
through  the  vessel,  or  the  degree  at  which  the  maximum 
oscillations  of  pressure  are  registered  by  the  manometer,  is 
taken  as  a  measure  of  the  blood  pressure  within. 

The  instruments  usually  employed  are  of  two  kinds — 

1.  Those  in  which  pressure  is  applied  to  the  walls  of  a 
superficial  artery,  such  as  the  radial,  by  a  small  rubber  bag 
distended  with  air  or  fluid,  and  connected  with  a  mano- 
meter, e.g.  those  of  Hill  and  Barnard  (small),  Oliver, 
Vierordt,  and  Von  Basch. 

2.  Those  in  which  pressure  is  applied  to  the  whole 
circumference  of  a  limb,  e.g.  the  arm,  by  a  large  rubber  bag 
which  completely  encircles  it,  e.g.  those  of  Riva  Rocci,  Hill 
and  Barnard  (large),  and  Gartner. 

In  both  groups  pressure  is  made  by  the  rubber  bag 
distended  with  air  or  fluid,  either  till  the  pulse  wave  below 
is  obliterated  or  till  maximum  oscillations  of  pressure  are 
attained.  The  former  indicates  the  systolic  pressure,  the 
latter  according  to  Jane  way  the  diastolic,  according  to  Hill  * 
the  mean  blood  pressure.  The  point  at  which  these  pheno- 
mena occur  is  read  off  on  a  manometer. 

It  would  be  out  of  place  to  discuss  these  instruments 
so  ably  described  by  Janeway,|  the  merits  and  demerits  of 
which  have  been  recently  reviewed  in  an  article  by  C.  J. 
Martin ;  %  but  it  may  be  well  to  point  out  why  the  deter- 
mination of  the  blood  pressure  by  these  methods  does  not 
give  a  trustworthy  estimate  of  the  arterial  tension.  The 
wall  of  the  vessel  varies  greatly  in  elasticity  and  thick- 
ness in  different  individuals  at  different  periods  of  life,  and 
in  health  and  disease,  and  the  varying  pressure  required  to 
overcome  the  resistance  of  the  arterial  wall  in  such  diverse 


*  "  Text-book  of  Physiology,"  edited  by  Scb'afer,  vol.  ii.  p.  80. 
t  "  The  Clinical  Study  of  Blood  Pressure  "  (Appleton). 
%  British  Medical  Journal,  1905,  vol.  i.  pp.  865  et  seq. 


24  HEART  DISEASE. 

conditions  must  prove  a  source  of  error.  Martin,  as  a 
result  of  a  series  of  experiments  on  portions  of  dead  arteries, 
claims  that  the  range  of  error  is  small,  and  that  an  approxi- 
mately accurate  allowance  can  be  made  in  the  case  of 
vessels  the  walls  of  which  are  rigid  from  degenerative 
changes.  Granting  that  this  is  so,  the  conditions  in  the 
living  vessel  are  essentially  different,  and  are  scarcely  com- 
parable. The  element  of  muscular  tone  in  the  vessel  wall 
must  be  taken  into  consideration.  When  the  arterial  ten- 
sion is  low  and  the  vessel  wall  normal,  this  is  perhaps  a 
negligible  quantity,  but  in  states  of  high  arterial  tension, 
such  as  are  associated  with  chronic  Bright's  disease,  there  is 
a  condition  of  overtone  or  contraction  of  the  muscular  coat 
almost  amounting  to  spasm,  and  the  resistance  to  compres- 
sion by  the  pneumatic  rubber  bag  offered  thereby  must  be 
very  considerable.  Moreover,  in  these  circumstances  there 
is  also  actual  hypertrophy  of  the  muscular  coat,  which  will 
intensify  this  resistance,  and  it  is  scarcely  possible  to  make 
accurate  allowance  for  these  sources  of  error,  which  will 
render  the  blood-pressure  reading  too  high.  Especially 
will  this  be  the  case  in  the  later  stages,  when  the  heart  is 
beginning  to  fail,  and  we  have  a  condition  of  comparatively 
low  blood  pressure  or  arterial  tension  associated  with  hyper- 
trophied  rigid  vessels,  difficult  to  compress. 

The  hypertrophy  of  the  muscular  coat  of  the  radial  or 
other  vessels  can  be  readily  demonstrated  post-mortem  by 
microscopical  examination  of  sections  of  the  vessel,  and 
I  have  never  failed  to  find  it  in  some  twenty  or  thirty 
cases  associated  with  granular  kidney  which  I  have  exam- 
ined. The  condition  of  overtone  or  hypertonus  is  not  so 
readily  proved,  though  it  can  be  readily  recognized  in 
life  by  a  practised  observer  by  careful  palpation  of  the 
vessel.  Dr.  William  Russell  *  has,  however,  demonstrated 
clinically  rhe  existence  of  this  hypertonus  by  an  ingenious 

*  Lancet,  1901,  vol.  i.  pp.  1519  et  seq. 


BLOOD  PRESSURE.  25 

experiment.  He  argues  that  if  this  condition  of  hypertonus 
exists  the  diameter  of  the  radial  artery  ought  to  vary 
according  to  the  degree  of  tone  or  contraction  of  the 
muscular  coat.  He  measured  the  diameter  of  an  artery  in 
a  state  of  hypertonus  by  Oliver's  arteriometer,  taking  at  the 
same  time  a  pulse  tracing.  He  then  gives  erythrol  tetra- 
nitrate  or  some  vaso-dilator,  and,  allowing  time  for  this  to 
take  effect,  he  again  measures  the  diameter  of  the  vessel  by 
the  arteriometer,  and  takes  another  pulse  tracing.  He  finds 
that  the  diameter  of  the  artery  is  increased  and  the  cha- 
racter of  the  pulse  altered  correspondingly  to  the  reduction 
of  tension. 

In  spite  of  these  sources  of  error,  the  determination  of 
the  blood  pressure  by  these  instruments  will  afford  a  useful 
comparative  estimate  of  the  blood  pressure  and  arterial 
tension,  and  this  may  with  advantage  be  supplemented  by 
sphygmographic  tracings.  The  scientific  results  obtained 
by  Oliver,  Mackenzie,  and  others  in  this  way  are  of  great 
value  and  interest.  It  is,  however,  not  always  practicable 
to  employ  instruments,  nor  is  it  essential  for  clinical  pur- 
poses, as  the  finger  can  by  practice  be  educated  so  that  a 
trustworthy  comparative  estimate  of  the  arterial  tension  can 
be  made.  For  this  purpose  three  fingers  should  be  placed 
on  the  radial  artery  and  varying  degrees  of  pressure  made. 
If  the  vessel  remains  full  between  the  beats  of  the  pulse, 
distended  by  the  contained  blood,  so  that  it  can  be  rolled 
like  a  cord  beneath  the  fingers,  the  mean  arterial  tension  is 
high.  Some  estimate  as  to  the  degree  may  be  inferred  from 
the  pressure  which  has  to  be  made  by  the  finger  before  the 
flow  of  blood  is  arrested  and  the  pulse  wave  obliterated. 
Care  must  be  taken  not  to  mistake  a  thickening  of  the 
arterial  wall  from  degenerative  changes  for  tension  due  to 
pressure  from  the  contained  blood.  In  cases  of  arterio- 
sclerosis the  condition  can  usually  be  diagnosed  from  the 
tortuous  brachial,  and  the  irregularity,  rigidity,  and  loss  of 


26  HEART  DISEASE. 

elasticity  of  the  vessel  wall,  which  is  quite  different  to 
the  firm,  cord-like,  smooth,  elastic  artery  in  a  condition  of 
hypertonus.  If  the  vessel  remains  soft  and  flaccid  between 
the  beats,  so  that  it  can  scarcely  be  felt,  it  is  obvious  that 
the  tension  or  blood  pressure  is  low. 

I  have  laid  some  stress  on  the  condition  of  hypertonus 
as  manifested  in  the  medium-sized  and  larger  arteries  as 
exemplified  in  the  radial,  but  it  exists  throughout  the 
arterial  system,  and  it  is  the  narrowing  of  the  vast  network 
of  arterioles  which  entails  a  great  increase  in  the  peripheral 
resistance  to  the  onward  flow  of  the  blood,  which  is  of  the 
first  importance.  The  increased  resistance  necessitates 
greater  driving  jDower  by  the  heart,  which  consequently 
hypertrophies  sometimes  to  an  enormous  degree.  The  blood 
pressure  is  of  necessity  correspondingly  raised,  and  the 
muscular  coat  of  the  large  and  medium-sized  arteries  hyper- 
trophies, or  they  would  give  way  under  the  strain. 

It  is  a  debatable  question  how  far  the  condition  of 
hypertonus  in  these  vessels  is  due  to  the  condition  akin  to 
spasm  which  affects  the  smaller  arterioles,  and  how  far  it  is 
a  natural  sequence  of  the  increased  peripheral  resistance. 
For  it  is  obvious  that  to  overcome  the  increased  resistance, 
increased  contractile  force  is  necessary,  not  only  on  the  part 
of  the  heart,  but  of  the  whole  arterial  system. 

This,  however,  is  a  matter  of  minor  importance  as  long 
as  we  recognize  that  increased  peripheral  resistance  entails 
increased  driving  power  by  the  heart  and  increased  con- 
tractile energy  by  the  larger  and  medium-sized  arteries. 
This  gives  rise  to  considerable  increase  in  the  blood  pres- 
sure, and,  consequently,  to  increased  strain  on  the  arterial 
walls,  or,  in  other  words,  to  high  arterial  tension.  When 
the  heart  begins  to  give  out  under  the  strain,  we  have  a 
decreased  blood  pressure  and  a  condition  of  low  or  moderate 
tension,  and  in  these  circumstances  we  must  be  careful  not 
to   mistake   the   resistance   offered   to   the  fingers  by  the 


HIGH  ARTERIAL    TENSION.  27 

hypertrophied  or   thickened  vessel  walls  for   one   of  high 
tension  due  to  high  pressure  from  within. 

The  Causes  of  Hypertonus  and  High  Arterial  Tension. — 
The  most  typical  instances  of  hypertonus  and  high  arterial 
tension  are  found  in  association  with  chronic  interstitial 
nephritis  or  granular  kidney.  A  reasonable  explanation  of 
the  mechanism  of  its  production  is,  that  poisonous  products 
are  retained  in  the  blood  as  the  result  of  imperfect  elimina- 
tion by  the  kidneys,  and  that  these  act  as  an  irritant  on 
the  walls  of  the  capillaries  and  arterioles,  setting  up  a 
reflex  spasm  or  hypertonic  condition  of  their  walls,  and 
creating  increased  peripheral  resistance. 

Of  predisposing  causes  heredity  is  the  most  important, 
and  we  see  the  tendency  to  high  tension  and  vascular  de- 
generation transmitted  from  generation  to  generation,  and 
sometimes  apparent  at  a  very  early  age. 

Certain  constitutional  diatheses,  gout,  diabetes,  and 
rheumatoid  arthritis,  are  frequently  associated  with  high 
arterial  tension.  Over- eating,  more  especially  excessive 
meat  eating,  in  those  hereditarily  predisposed  may  be  a 
cause,  and  it  is  probable  that  in  this  instance  and  in  gout, 
perverted  or  defective  metabolism,  with  resulting  absorption 
of  toxic  products  into  the  blood,  and  imperfect  elimination, 
are  the  important  etiological  factors. 

In  the  later  stages  of  pregnancy  the  blood  pressure  is 
raised,  and  in  the  affection  known  as  eclampsia  the  arterial 
tension  is  always  extremely  high.  The  explanation  of  this 
condition  would  seem  to  be  that  though  the  kidneys  are  not 
diseased,  the  extra  work  of  eliminating  the  waste  products 
of  the  foetus  in  addition  to  those  of  the  mother  is  too  much 
for  them,  and  toxic  products  accumulate  in  the  blood,  as  in 
the  case  of  granular  kidney,  and  produce  similar  phenomena. 

Lead  poisoning  is  unquestionably  an  important  and 
common  cause.  Alcohol  and  tobacco  have  been  incrimi- 
nated, but  the  part  played  by  them  is  doubtful.     Since  the 


28  HEART  DISEASE. 

discovery  of  the  tonic  action  of  adrenalin  on  the  arterial 
system,  it  has  been  suggested  that  excessive  secretion  of 
the  suprarenal  glands  may  be  a  cause,  but  there  is  no  evi- 
dence in  support  of  this.  Whatever  be  the  underlying 
cause  of  high  arterial  tension,  it  seems  probable  that  it  acts 
by  generating  increased  peripheral  resistance  in  the  smaller 
arterioles  and  capillaries. 

Confusion  has  arisen  by  mistaking  the  condition  of 
hypertonus  and  hypertrophy  of  the  muscular  coat  of  the 
artery  for  arterio-sclerosis  or  degenerative  change,  because 
the  artery  feels  hard  and  cord-like.  But  in  the  majority  of 
cases,  in  the  earlier  stages,  the  radial  artery  will,  on  micro- 
scopic examination,  be  found  to  be  perfectly  normal  except 
for  hypertrophy  of  the  media. 

Later  on  degenerative  changes  set  in  in  the  hyper- 
trophied  vessels,  and  patches  of  atheroma  or  necrosis  will 
be  found  in  the  sub-endothelial  tissue,  possibly  as  a  result 
of  the  prolonged  strain  and  impaired  nutrition,  or  due  to 
the  action  of  the  toxins  which  have  given  rise  to  the  high 
tension.  Of  these,  lead  is  especially  prone  to  give  rise  to 
early  vascular  degeneration.  The  arteries  most  affected  are 
usually  the  cerebral,  the  coronary  arteries  of  the  heart,  and 
the  aorta,  so  that  the  patient,  if  he  escapes  the  perils  of 
uraemia,  is  liable  to  succumb  to  cerebral  hemorrhage,  or  to 
cardiac  failure  from  degenerative  changes  in  the  heart,  or 
to  aneurysm  of  the  aorta. 


CHAPTER    III. 
DISEASES   OF   THE  PERICARDIUM. 

PERICARDITIS  —  MORBID  ANATOMY  —  ETIOLOGY  —  PHYSICAL 
SIGNS — SIGNS  OF  EFFUSION  AND  CARDIAC  DILATATION — 
SYMPTOMS — COURSE  OF  THE  DISEASE — DIFFERENTIAL 
DIAGNOSIS — PROGNOSIS  :  TREATMENT — ADHERENT  PERI- 
CARDIUM —  SUPPURATIVE  PERICARDITIS  —  HYDROPERI- 
CARDIUM — PNEUMOPERICARDIUM,  ETC. 

The  pericardium  is  a  nbro-serous  sac  which  envelops  the 
heart.  The  fibrous  portion  is  pyramidal  in  shape,  and  at 
its  base  is  firmly  attached  to  the  central  tendon  of  the 
diaphragm  and  the  adjoining  muscular  substance ;  above 
it  is  continued  as  a  tubular  prolongation  on  to  the  root  of 
the  aorta  and  pulmonary  artery,  and  is  gradually  lost  in 
the  connective  tissue  of  their  external  coats.  The  serous 
membrane  lining  the  sac,  termed  the  parietal  layer  of 
pericardium,  passes  up  to  the  root  of  the  great  vessels, 
which  it  envelops  in  a  common  sheath  for  an  inch  to  an 
inch  and  a  half  from  their  origin,  and  is  thence  reflected 
on  to  the  surface  of  the  heart,  which  it  closely  invests, 
constituting  the  visceral  layer  of  pericardium.  Laterally 
and  anteriorly,  save  for  a  small  triangular  area  in  front 
termed  the  anterior  mediastinum,  the  pericardium  is  in 
contact  with  the  pleura ;  posteriorly  it  is  in  relation  with 
the  oesophagus,  aorta,  trachea,  and  the  root  of  the  left 
lung.  The  phrenic  nerves  pass  down,  one  on  either  side 
of  the  sac. 


3°  HEART  DISEASE. 

Morbid  Anatomy. — In  the  early  stages  the  pericardium 
becomes  hyperseinic  and  congested.  Then  exudation  of 
serum  and  leucocytes  takes  place  from  the  congested 
vessels,  and  soon  both  visceral  and  parietal  layers  of  peri- 
cardium become  coated  in  patches  or  throughout  their 
surface  with  a  thick  layer  of  yellow  sticky  lymph.  From 
the  friction  together  of  the  two  inflamed  surfaces  the 
lymph  coating  them  acquires  an  irregular,  ragged,  or 
honeycomb  appearance.  The  lymph  on  the  surface  of  the 
pericardium  may  be  reabsorbed,  but  frequently  becomes 
vascularized  and  organized  into  fibrous  tissue,  gluing 
together  the  two  layers  of  pericardium  where  they  come 
into  contact,  and  giving  rise  to  partial  or  universal  adhesion 
between  the  heart  and  pericardium. 

Effusion  may  take  place  into  the  pericardial  sac  to  a 
varying  extent.  Usually  it  is  small  in  amount,  but  excep- 
tionally it  may  be  very  large.  In  rheumatic  cases  a  large 
effusion  is  uncommon. 

The  effusion  consists  of  a  yellowish  serous  fluid  in 
which  leucocytes,  shreds  of  fibrin,  and  endothelial  cells 
are  present  in  varying  quantity.  The  fluid  is  usually  clear, 
but  may  be  turbid  if  there  is  much  cellular  exudation,  and 
may  contain  flakes  of  lymph.  Sometimes  it  is  blood- 
stained, and  in  scurvy  may  consist  almost  entirely  of 
blood. 

It  may  from  the  outset  be  purulent,  constituting  "  sup- 
purative pericarditis,"  which  differs  so  materially  in  its 
clinical  features  from  the  simple  plastic  or  fibrinous  form 
that  its  consideration  will  be  reserved  for  another  section. 

"  Milk  spots,"  or  white  opaque  patches  sometimes  found 
at  autopsies  on  the  surface  of  the  visceral  pericardium,  are 
not,  as  a  rule,  due  to  pericarditis,  but  to  a  localized  growth 
of  connective  tissue  from  irritation,  and  they  occur  at  some 
point  where  the  heart  in  its  movements  comes  into  contact 
with  the  chest  wall. 


DISEASES  OF  THE  PERICARDIUM.  31 

The  Myocardium. — The  heart  muscle  is  almost  invariably 
affected,  and  there  is  myocarditis  to  a  varying  degree,  with 
resulting  granular  and  fatty  degeneration  of  the  muscle 
fibres.  In  the  more  protracted  cases  areas  of  round-celled 
infiltration  may  sometimes  be  found  in  the  interstitial 
tissue  between  the  muscle  fibres. 

It  is  to  this  accompanying  myocarditis  that  we  must 
attribute  the  cardiac  dilatation  which  is  so  marked  a  feature 
in  pericarditis.  One  of  the  chief  dangers  in  rheumatic 
inflammation  of  the  heart,  of  which  pericarditis  is  a  part, 
lies  in  the  damage  to  the  cardiac  muscle. 

Etiology. 

Rheumatism  is  by  far  the  most  common  and  important 
cause  of  pericarditis.  So  close  is  the  connection  between 
the  two  that,  as  Dr.  Frederick  Roberts  says,*  "The  peri- 
cardial inflammation  is  not  to  be  looked  upon  as  a  mere 
complication  of  rheumatism,  but  is  an  integral  part  of  the 
disease."  Furthermore,  pericarditis  must  not  be  regarded 
as  a  separate  entity,  but  as  part  of  a  general  inflammation  of 
the  heart,  aptly  termed  "  carditis  "  by  the  late  Dr.  Sturges,t 
the  myocardium  being  almost  invariably,  and  the  endo- 
cardium frequently,  affected.  Pericarditis  occurring  in  asso- 
ciation with  chorea  may  be  regarded  as  of  rheumatic  origin. 

Rheumatism. — In  childhood  and  early  adolescence  rheu- 
matism is  especially  liable  to  attack  the  heart,  while  the 
joints  may  be  so  slightly  affected  that  attention  is  not 
drawn  to  them.  In  later  life  the  joints  are  more  apt  to 
suffer  severely  while  the  heart  frequently  escapes. 

The  belief  has  long  been  held  that  acute  rheumatism 
is  a  disease  of  microbic  origin,  and  that  pericarditis  and 
endocarditis  are  local  manifestations  of  the  activity  of  a 
specific  micro-organism.     From  the  experimental  researches 

*  Allbutt's  "  System  of  Medicine,"  vol.  v.  p.  752. 
f  Lumleiau  Lectures,  189L 


32  HEART  DISEASE. 

of  Triboulet,  Wasserman,  Paine  and  Poynton,  Shaw,  Ainley, 
Walker,  Beattie,  and  others,  it  would  appear  that  acute 
rheumatism  is  due  to  a  minute  diplococcus,  which  may- 
grow  in  chains  like  a  streptococcus.  This  micro-organism 
they  have  succeeded  in  isolating  from  the  pericardial  fluid 
and  blood  of  patients  suffering  from  rheumatic  fever,  and, 
after  growing  it  on  suitable  culture  media,  have  inoculated 
it  into  rabbits  and  reproduced  pericarditis,  arthritis,  and 
endocarditis,  or  a  disease  indistinguishable  from  acute  rheu- 
matism. Pericarditis,  therefore,  occurring  in  association 
with  rheumatism,  may  be  regarded  as  due  to  a  micro- 
organism. The  question  as  to  whether  this  is  the  specific 
micro-organism  of  rheumatism,  is  further  discussed  in  the 
chapter  on  acute  endocarditis. 

Pneumonia. — Pericarditis  may  occur  as  a  complication 
of  pneumonia  or  pleurisy,  or  even,  in  the  absence  of  these 
affections  as  a  primary  disease,  from  infection  by  the  pneumo- 
coccus,  which  can,  as  a  rule,  be  readily  isolated  from  the 
fluid  in  the  pericardium  in  cases  of  pneumococcal  origin. 

The  Acute  Specific  Diseases.  —  Acute  pericarditis  may 
ensue  as  a  complication  of  scarlet  fever,  variola,  erysipelas 
— rarely  of  measles  and  typhus  fever. 

Bright's  Disease. — Pericarditis  is  met  with  in  Bright's 
disease  most  commonly  in  association  with  the  later  stages 
of  granular  kidney  or  subacute  parenchymatous  nephritis. 

Traumatism. — Injuries  to  the  pericardium  by  a  gunshot 
or  punctured  wound,  or  by  a  fractured  rib,  or  by  a  fish-bone 
lodged  in  the  cesophagus,  may  set  up  pericarditis. 

Tubercular  pericarditis  may  occur  as  part  of  a  general 
miliary  tuberculosis,  or  from  the  extension  of  the  disease 
from  a  tubercular  lung  or  bronchial  gland. 

Physical  Signs. 

Friction  rub. — The  most  trustworthy  sign  of  pericarditis 
is   the  characteristic   to-and-fro  friction   sound   heard    on 


DISEASES  OF  THE   PERICARDIUM.  33 

auscultation.  For  this  reason,  auscultation  will  be  considered 
before  percussion.  The  friction  sound  is  caused  by  the 
rubbing  together  of  the  two  inflamed  surfaces  of  the  peri- 
cardium at  each  beat  of  the  heart.  It  is  a  curious  scratching 
rub  which  appears  to  be  very  superficial,  and  somewhat 
resembles  the  noise  made  by  scratching  a  piece  of  rough 
paper  with  the  finger-nail.  It  is  modified  by  pressure  with 
the  stethoscope,  and  may  be  rendered  more  distinct  and 
longer  or  almost  extinguished.  It  is  usually  of  a  to- 
and-fro  character,  corresponding  more  or  less,  but  not 
accurately,  to  the  movements  of  the  heart  in  systole  and 
diastole.  It  may  be  only  systolic  in  time  and  not  present 
the  to-and-fro  character ;  this  is  usually  the  case  when 
it  is  heard  near  the  apex,  and  not  over  the  base.  On  the 
other  hand,  over  the  base  of  the  heart  the  friction  sound 
may  be  triple  or  cantering  instead  of  merely  to  and  fro,  the 
auricular  systole  being  attended  with  an  audible  inde- 
pendent rub.  It  is  said  to  be  first  heard,  as  a  rule,  over 
the  base  of  the  heart,  but  frequently  it  is  first  audible  at 
the  apex  as  a  single  scratch  at  each  systole.  As  the  in- 
flammation spreads,  a  to-and-fro  friction  rub  is  heard  over 
the  whole  or  a  large  proportion  of  the  precordial  area,  and 
since  the  heart  is  usually  dilated  it  may  be  heard  an  inch 
or  more  to  the  right  of  the  sternum  in  children.  The  rub 
may  be  present  for  a  day  or  two  only  in  mild  cases ;  in 
cases  of  effusion  it  may  be  present  for  a  few  days,  then 
disappear  and  reappear  when  the  fluid  is  absorbed  or  drawn 
off  by  paracentesis.  In  subacute  or  chronic  cases  the  rub 
persists  for  some  days  or  weeks,  only  disappearing  as  the 
layers  of  pericardium  become  adherent. 

Disappearance  of  the  rub  may  thus  indicate  (1)  sub- 
sidence of  the  attack ;  (2)  effusion  into  the  pericardium ; 
(3)  formation  of  adhesion  between  the  two  layers  of  the 
pericardium. 

Friction  fremitus    may   be   felt   on   palpation   in   well- 

D 


34  HEART  DISEASE. 

marked  cases  over  the  area  where  the  friction  sound  is  best 
heard. 

The  action  of  the  heart  is  excited  and  the  pulse  almost 
invariably  accelerated,  as  a  rule,  before  the  friction  rub 
becomes  audible.  Sometimes  in  children  it  may  be  irregular 
in  rhythm  for  a  time.  After  the  friction  rub  has  apjDeared, 
a  peculiar  triple  cantering  rhythm  of  the  heart  is  frequently 
heard  on  auscultation  at  the  apex,  and  is  very  characteristic. 
It  is  apparently  due  to  reduplication  of  the  first  sound. 

Increase  in  the  Aeea  of  Caediac  Dulness. 

Increase  in  the  area  of  cardiac  dulness  is  usually  one 
of  the  earliest  physical  signs.  This  is  especially  marked 
in  children,  in  whom  it  is  most  easily  mapped  out  on 
percussion.  It  is  more  rapid  and  extensive  in  proportion 
to  the  severity  and  acuteness  of  the  attack.  The  dulness  may 
extend  upwards  as  far  as  the  second  left  intercostal  space, 
and  outwards  for  an  inch  outside  the  vertical  nipple  line, 
and  in  the  opposite  direction  for  an  inch  or  more  to  the 
right  of  the  sternum,  but  it  is  usually  not  so  extensive  in 
adults  as  in  children,  and  is  less  easily  made  out,  because 
of  the  thickness  of  the  chest  wall  and  errors  that  may 
arise  from  pathological  conditions  in  the  lungs. 

The  view  was  held  by  Sibson  *  that  this  increase  in  the 
area  of  cardiac  dulness  indicates  pericardial  effusion,  and 
that  increase  in  effusion  is  indicated  by  extension  of  the 
cardiac  dulness.  In  a  certain  proportion  of  cases  this  is 
undoubtedly  true  ;  but  much  evidence  has  been  accumulated 
which  tends  to  show  that  this  is  by  no  means  the  rule, 
and  that  the  increase  in  dulness  indicates  in  the  large 
majority  of  cases  of  rheumatic  pericarditis,  increase  in  the 
size  of  the  heart,  or  cardiac  dilatation. 

In  1895,  in  a  monograph  on  "  Adherent  Pericardium," 

*  Sibson'e  Works,  edited  by  Ord. 


DISEASES  OF  THE  PERICARDIUM.  35 

I  described  a  series  of  cases  where  marked  increase  in 
the  area  of  cardiac  dulness  was  found,  post-mortem,  to 
be  due,  not  to  effusion,  but  to  cardiac  dilatation.  In  two 
cases  where  the  physical  signs  and  symptoms  seemed  to 
point  conclusively  to  considerable  pericardial  effusion 
paracentesis  was  resorted  to,  but  in  neither  instance  was 
fluid  found,  and  the  increase  in  dulness  was  found  to  be 
due  to  increase  in  the  size  of  the  heart. 

Lees  and  Poynton  *  drew  attention  to  the  acute  dilata- 
tion of  the  heart  that  occurs  in  the  rheumatism  and  chorea 
of  childhood.  From  an  analysis  of  the  post-mortem  records 
of  150  cases  of  fatal  rheumatic  heart  disease  in  children, 
they  showed  that  cardiac  dilatation  is  usually  present,  and 
marked  excess  of  pericardial  fluid  rare  ;  in  only  12  cases 
out  of  150  was  there  excess  of  pericardial  fluid  amounting 
to  more  than  two  ounces. 

Out  of  79  cases  of  paracentesis  pericardii,  collected  by 
Dr.  Samuel  West,f  only  11  were  of  rheumatic  origin,  and 
in  only  one  of  these  eleven  was  the  effusion  large  in 
amount. 

Clinically,  it  is  not  an  uncommon  experience,  even 
when  the  area  of  cardiac  dulness  is  very  much  enlarged, 
extending  to  the  right  of  the  sternum,  to  hear  a  pericardial 
rub  at  several  points  over  the  dull  area.  This  seems  incom- 
patible with  the  presence  of  fluid,  and  in  many  of  these  cases, 
at  the  post-mortem,  no  excess  of  pericardial  fluid  is  found, 
but  a  dilated  heart  with  the  pericardium  partially  adherent. 
Effusion. — In  effusion  the  outline  of  the  area  of  cardiac 
dulness  tends  to  assume  a  pyramidal  or  pyriform  shape, 
with  the  base  or  widest  portion  below.  The  transition 
from  the  dull  area  to  the  resonant  lung  is  sudden  and 
well-marked,   and   the   extent   and   shape   of   the   area   of 

*  Trans.  Med:  Chi.  Soc,  June,  1898. 

t  West,  S.,  "  Paracentesis  Pericardii,"  Trans.  Med.  Chi.  Soc,  vol.  66, 
p.  235. 


36  HEART  DISEASE. 

cardiac  dulness  will  vary  somewhat  with  the  position  of 
the  patient. 

Sibson  gave  a  series  of  diagrams  to  illustrate  the  shape 
assumed  by  the  pericardial  sac  in  the  different  stages  of 
effusion,  but  it  is  doubtful  how  far  these  are  of  practical 
value  for  differential  diagnosis,  as  they  were  not  confirmed 
by  post-mortem  examination,  and  he  appears  to  have 
taken  it  for  granted  that  increase  in  the  area  of  cardiac 
dulness  invariably  indicated  effusion.  It  is,  however,  by 
no  means  an  easy  matter  to  decide  by  percussion  alone, 
whether  the  increased  area  of  dulness  indicates  effusion, 
cardiac  dilatation,  or  dilated  heart  with  the  pericardium 
adherent. 

There  is  much  diversity  of  opinion  as  to  the  position 
assumed  by  the  heart  in  effusion.  Sibson  maintained  that 
it  was  usually  pushed  upwards  and  outwards,  and  the  apex 
beat  similarly  displaced ;  but  this  is  not  invariably  the  case, 
and  pericardial  adhesions  may  fix  the  apex  in  various  positions, 
and  in  effusion  of  any  extent  it  is  not  as  a  rule  palpable. 

Bulging  of  the  precordial  area  as  a  whole,  more 
especially  of  the  intercostal  spaces  over  this  area,  which  is 
usually  best  marked  in  purulent  pericarditis,  is  a  more 
trustworthy  sign  of  effusion. 

Gradual  enfeeblement  of  the  apex  beat  from  day  to 
day,  or  even  its  eventual  disappearance,  together  with 
increasing  weakness  and  distance  of  the  sounds  heard 
at  the  apex,  especially  if  there  is  at  the  same  time  an 
increase  in  the  severity  of  the  symptoms,  and  marked 
dyspnoea,  are  strongly  suggestive  of  increasing  effusion 
into  the  pericardium. 

Symptoms. 

The  symptoms  are  partly  local,  due  to  the  pericarditis 
itself,  and  partly  constitutional,  or  due  to  a  general  toxamiia. 


DISEASES  OF  THE  PERICARDIUM.  37 

Pain  in  the  precordial  region,  increase  in  the  pulse- 
rate,  excited  action  of  the  heart,  dyspnoea  varying  in  degree, 
rise  of  temperature,  restlessness  at  night,  are  symptoms 
usually  well  marked  in  acute  pericarditis  ;  but  in  the  sub- 
acute variety,  common  in  children,  there  may  be  little  or 
no  pain  or  fever,  and  very  slight  dyspnoea,  though  there  is 
usually  acceleration  of  the  pulse.  The  symptoms,  as  a 
rule,  precede  the  development  of  the  pericardial  rub,  and 
are  more  marked  when  it  appears.  In  children  there 
may  be  premonitory  symptoms  of  nervous  origin,  such  as 
night  terrors,  crying  out,  and  wandering  in  sleep,  restless- 
ness, and  even  slight  delirium  on  first  waking.  Vomiting 
may  set  in,  and  is  generally  of  serious  prognostic  signifi- 
cance. The  face  may  be  pale  or  flushed,  the  expression  is 
often  anxious  or  distressed,  and  the  respiration  hurried. 
There  may  be  some  pain  or  difficulty  in  swallowing  from 
the  proximity  of  the  pericardium  to  the  oesophagus,  if  the 
posterior  aspect  is  inflamed,  or  if  there  is  much  effusion 
into  the  sac.  The  temperature  ranges  between  100°  and 
103°,  and  is  usually  higher  in  adults  than  in  children,  in 
whom  the  attack  is  commonly  less  acute  and  more  insidious 
in  its  onset.  The  dyspnoea  may  become  very  considerable, 
not  only  in  cases  of  effusion,  but  in  cases  where  there  is 
great  cardiac  dilatation  and  the  pericardium  is  becoming 
adherent ;  the  patient  has  to  be  propped  up  with  pillows, 
and  when  there  is  much  effusion  or  extreme  dilatation  of 
the  heart,  may  find  most  comfort  in  leaning  forward  over  a 
bed-board,  with  his  head  on  his  hands. 

In  severe  cases,  nervous  symptoms  may  predominate, 
and  there  may  be  delirium,  involuntary  passage  of  motions 
and  urine,  great  restlessness,  or  a  state  resembling  collapse. 
Vomiting  is  always  a  serious  symptom,  and  not  infrequently 
ushers  in  the  closing  scene. 


3§  heart  disease. 

Course  of  the  Disease  and  Terminations. 

The  disease  as  a  rule  runs  a  somewhat  different 
course  in  adults  and  in  children.  In  adults  it  is  usually 
acute,  and  the  symptoms  are  more  marked  at  the  onset ;  in 
children  it  may  from  the  first  be  sub-acute  or  chronic 
in  character,  and  it  results  frequently  in  the  formation  of 
adhesions  between  the  heart  and  pericardium.  It  must 
not  be  forgotten  that  the  prognosis  to  a  great  extent 
depends  on  the  degree  to  which  the  cardiac  muscle  is 
attacked  by  the  inflammatory  process.  In  very  severe 
attacks  death  may  ensue  within  two  or  three  days  from 
the  time  at  which  the  disease  is  first  recognizable  by  the 
pericardial  rub.  In  such  cases  there  is  usually  rapid  in- 
crease in  the  area  of  cardiac  dulness,  and  in  the  severity 
of  symptoms,  and  sometimes  attacks  of  vomiting.  Post- 
mortem there  is  commonly  little  or  no  effusion  beyond  the 
lymph  on  the  serous  surfaces,  but  great  cardiac  dilatation, 
and  it  would  seem  as  if  the  severity  of  the  inflammation 
had  caused  paresis  of  the  cardiac  muscle,  analogous  to  that 
which  occurs  in  the  muscular  coats  of  the  intestines  in 
acute  peritonitis. 

In  a  mild  case,  though  the  symptoms  at  the  onset  may 
be  severe,  the  friction  rub  persists  for  a  few  days  only, 
23erhaps  not  more  than  one  or  two ;  the  area  of  cardiac 
dulness  does  not  greatly  increase,  and  rapidly  decreases  to 
normal  when  the  friction  rub  has  disappeared  :  convalescence 
is  soon  established.  In  the  more  severe  type  of  acute  cases, 
effusion  may  occur,  and  require  removal  by  paracentesis. 

In  the  sub-acute  type,  common  in  children,  the  onset 
is  insidious,  and  the  symptoms  are  ill  marked.  The  friction 
rub  may  persist  for  some  days  or  weeks,  the  area  of 
cardiac  dulness  becomes  greatly  enlarged,  and  remains 
so  permanently,  and  eventually,  when  the  friction  rub 
disappears,  the  pericardium  is  left  partially  or  universally 


DISEASES   OF  THE  PERICARDIUM.  39 

adherent  to  the  heart.  The  child,  even  after  convales- 
cence is  established,  remains  pale  and  thin,  is  short  of 
breath,  and  incapable  of  exertion,  as  the  heart  with  its 
mnscle  damaged  by  myocarditis  and  hampered  by  pericardial 
adhesions,  remains  permanently  crippled. 

In  another  class  of  sub-acute  cases  where  the  inflam- 
matory process  persists  for  some  months,  or  repeated  attacks 
in  close  succession  ensue,  dropsy  may  supervene,  the  liver 
becoming  enlarged  and  the  cardiac  dilatation  extreme,  the 
patient  dying  with  all  the  symptoms  of  cardiac  failure  from 
extensive  damage  to  the  cardiac  muscle  by  myocarditis. 

As  an  illustration  of  the  life  history  of  such  a  case,  the 
following  may  be  quoted  : — 

H.  D.,  set.  9,  was  admitted  to  the  Children's  Hospital? 
Great  Orrnond  Street,  11th  December,  1893,  with  a  history 
of  pains  in  the  joints,  fourteen  days  previous  to  his  admission. 
When  first  seen,  his  heart  was  considerably  dilated,  and  a 
mitral  systolic  murmur  was  audible  at  the  apex.  Five 
days  after  admission  a  pericardial  rub  was  heard,  which 
persisted  for  about  a  week,  during  which  time  the  cardiac 
dilatation  increased.  A  week  later  he  began  to  improve, 
and  the  area  of  cardiac  dulness  gradually  decreased.  On 
the  15th  February,  1894,  two  months  after  the  onset  of  the 
pericarditis,  the  area  of  cardiac  dulness  was  almost  normal 
in  extent,  and  he  was  sufficiently  recovered  to  go  to  a  con- 
valescent home.  A  month  later,  he  had  a  fresh  attack  of 
rheumatism  with  an  eruption  of  nodules,  and  was  readmitted 
15th  March ;  there  was  slight  oedema  of  the  legs,  and 
rheumatic  nodules  were  present  on  the  elbows ;  the  area  of 
cardiac  dulness  was  again  greatly  enlarged,  and  he  suffered 
from  severe  dyspnoea.  From  this  time  he  steadily  got 
worse,  the  oadema  of  the  legs  rapidly  increased,  the  liver 
became  greatly  enlarged,  the  veins  of  the  neck  distended 
and  pulsating,  and  he  died  on  the  21st  April,  with  extreme 
symptoms    of    venous    engorgement    and    right    ventricle 


40  HEART  DISEASE. 

failure.  At  the  post-mortem  all  the  cavities  of  the  heart 
were  greatly  dilated ;  the  pericardium  was  universally 
adherent  by  recent  adhesions,  the  muscle  was  soft,  and 
showed  evidence  microscopically  of  myocarditis  ;  there  was 
no  serious  valvular  lesion,  though  a  few  vegetations  were 
present  on  the  mitral  valve,  and  its  orifice  was  much 
dilated.  Myocarditis  and  adherence  of  the  pericardium  to 
the  dilated  heart  were  thus  responsible  for  his  death.  The 
symptoms  were  those  of  venous  engorgement  and  right 
ventricle  failure,  as  the  right  ventricle  with  its  comparatively 
thin  walls  was  more  rapidly  rendered  helpless  by  the  myo- 
carditis, and  more  hampered  by  the  adherent  pericardium 
than  the  left,  with  its  greater  thickness  of  muscular  tissue. 

Effusion  of  any  extent  is  rare  in  the  sub-acute  rheumatic 
cases  in  children,  adhesions,  partial  or  universal,  between 
the  heart  and  pericardium  being  the  most  common  termina- 
tion. Effusion  is  more  likely  to  occur  in  acute  attacks 
in  adults,  especially  those  associated  with  pneumonia  or 
Bright's  disease,  and  effusion  of  blood  into  the  pericardium 
is  common  in  scurvy. 

Diagnosis. 

Till  the  pericardial  friction  rub  is  heard,  a  certain 
diagnosis  of  pericarditis  cannot  be  made.  Usually,  how- 
ever, in  acute  attacks  there  are  premonitory  symptoms,  such 
as  pain  in  the  precordial  region,  restlessness,  dyspnoea, 
acceleration  of  pulse,  and  rise  of  temperature  which  enable 
us  in  some  measure  to  anticipate  the  appearance  of  the 
friction  rub.  These  symptoms  may  in  some  cases  appear 
to  be  only  exacerbations  of  those  already  existing,  as  the 
result  of  rheumatism,  pneumonia,  or,  possibly,  scarlet  fever, 
but  as  the  patient  is  then  confined  to  his  bed,  we  shall  be 
on  the  look-out  for  cardiac  complications,  and  are  not 
Hkely  to  miss  the  first  definite  signs  of  pericarditis. 

The  sub-acute  attacks  so  common  in  children  are.  on  the 


DISEASES  OF  THE  PERICARDIUM.  41 

contrary,  as  a  rule,  very  insidious  in  their  onset,  and  the 
child  may  be  going  about  with  pericarditis,  especially  in 
the  eyent  of  a  second  attack,  before  the  symptoms  are  so 
severe  as  to  attract  attention  to  the  child's  condition,  and 
cause  the  parents  to  seek  medical  advice,  or  the  physician 
to  examine  the  heart.  Much  damage  may  thus  be  done  to 
the  heart  before  the  existence  of  pericarditis  is  discovered. 

The  articular  manifestations  of  rheumatism  in  children 
are,  moreover,  slight,  as  a  rule,  while  the  heart  is  commonly 
attacked.  It  is  important,  therefore,  not  to  neglect  the 
slightest  evidence  of  rheumatism  in  children,  and  if  we 
have  reason  to  suspect  its  existence,  to  keep  a  careful  watch 
over  the  child,  and  examine  the  heart  at  frequent  intervals. 

Differential  Diagnosis. 

A  friction  rub  due  to  pleurisy  in  the  neighbourhood  of 
the  heart  will  be  readily  distinguished  by  the  fact  that 
its  rhythm  is  synchronous  with  the  respiratory  movements, 
and  not  with  those  of  the  heart.  Some  difficulty  may, 
however,  arise  when,  from  friction  between  the  pericardium 
and  the  pleura  overlapping  or  adjoining  it,  the  rhythm  is 
of  a  to-and-fro  character  corresponding  to  the  beats  of  the 
heart.  A  friction  rub  arising  from  this  cause  will  be 
intensified  by  the  respiratory  movements,  and  will  usually 
be  extinguished  when  the  breath  is  held  in  deep  inspiration. 
It  will,  as  a  rule,  be  heard  only  at  the  left  border  of  the 
heart  over  the  ventricles,  and  not  at  the  base  of  the  heart, 
or  to  the  right  of  the  sternum.  Moreover,  as  the  pleurisy 
will  seldom  be  confined  to  the  precordial  region,  a  well- 
marked  respiratory  friction  rub  will  usually  be  heard  in 
the  adjoining  area. 

Endocardial  murmurs  differ  so  completely  in  their 
character  from  pericardial  friction  sounds,  that  confusion 
will  seldom  arise.  They  will  not,  of  course,  be  modified 
by  pressure  with  the  stethoscope. 


HEART  DISEASE. 


Pkognosis. 


Pericarditis  is  always  a  disease  of  considerable  gravity 
owing  to  the  myocarditis  which  usually  accompanies  it. 
In  acute  attacks,  associated  with  rheumatism  or  pneumonia, 
death  may  take  place  within  the  first  few  days,  but  this 
is  not  a  common  occurrence.  In  a  large  proportion  of 
rheumatic  cases  the  immediate  prognosis  is  favourable, 
though  the  liability  to  repeated  attacks,  the  probable 
damage  to  the  heart  by  myocarditis,  and  the  formation  of 
adhesions  between  the  heart  and  pericardium,  render  the 
ultimate  chances  of  long  life  unfavourable.  When  associ- 
ated with  Bright's  disease,  the  prognosis  is  usually  bad,  and 
the  chance  of  recovery  small. 

In  sub- acute  and  prolonged  cases  the  prognosis  seems  to 
depend  on  the  degree  to  which  the  myocardium  is  affected 
bv  the  inflammatory  process.  If  the  inflammation  is  of 
short  duration  and  the  changes  in  the  muscle  are  slight,  the 
heart  may  rapidly  contract  down  again  to  its  normal  size, 
and  be  little  the  worse ;  if  the  inflammation  is  protracted 
and  severe,  involving  great  destruction  of  the  myocardium, 
the  heart  is  unable  to  recover  for  some  time,  and  in  the 
process  of  repair  fibrous  tissue  takes  the  place  of  the  damaged 
muscle,  so  the  heart  is  permanently  weakened.  The  peri- 
cardium may  also  become  adherent  to  it. 

Children,  once  attacked,  are  liable  to  repeated  and  pro- 
longed attacks  of  cardiac  inflammation,  both  pericardial, 
myocardial,  and  endocardial.  They  seldom  grow  up  to 
maturity ;  or,  if  they  do,  it  is  with  hearts  so  crippled  that 
they  do  not  survive  many  years. 

Adults  attacked  by  pericarditis  usually  fare  better  than 
children,  for  though  the  symptoms  are  usually  more  acute 
at  the  time  of  the  attack,  its  duration  is  short,  and  the  heart 
often  seems  to  escape  without  serious  damage. 


diseases  of  the  pericardium.  43 

Tkeatment. 

In  the  treatment  of  pericarditis  various  local  applications, 
such  as  ice-bags,  leeches,  or  blisters  over  the  prsecordial 
area,  have  been  advocated.  Of  these,  ice-bags  are  the  most 
useful,  as  they  relieve  pain  in  acute  pericarditis,  and,  accord- 
ing to  Lees,  modify  the  inflammation  and  limit  the  dila- 
tation of  the  heart.  Leeches  are  often  of  service  at  the  outset 
of  pericarditis,  and  may  be  followed  by  ice-bags ;  blisters 
are  better  suited  for  the  later  and  more  chronic  stages.  The 
administration  of  salicylates,  which  in  the  acute  articular 
rheumatism  of  adults  are  given  with  such  marked  beneficial 
results,  is  of  doubtful  service.  If  the  pain  is  severe,  opium 
or  morphia  may  be  given  with  marked  benefit ;  if  stimulants 
are  required,  brandy,  ammonia,  and  ether,  or  strychnine, 
may  be  given.  Digitalis,  and  similar  cardiac  tonics,  should 
not  be  given  during  the  acute  stage.  As  a  general  tonic, 
an  effervescing  mixture,  containing  quinine  and  bicarbonate 
of  potash,  is  perhaps  as  useful  as  any.  Nothing,  however, 
in  severe  cases  seems  to  arrest  or  exert  any  controlling 
influence  on  the  course  of  cardiac  inflammation  in  children, 
when  once  it  has  gained  a  firm  hold.  It  is,  therefore,  of 
the  first  importance  that  any  indications  of  danger  threaten- 
ing the  heart  should  be  recognized  as  early  as  possible, 
and  due  precautions  taken.  If,  then,  a  suspicion  of  rheu- 
matism is  aroused  by  complaints  of  stiffness  in  the  joints 
or  pains  in  the  limbs,  in  a  child  who  comes  of  a  rheumatic 
stock,  or  who  has  previously  suffered  from  chorea  or  some 
other  rheumatic  manifestation,  more  especially  if  rheumatic 
nodules  are  present,  the  patient  should  be  kept  under 
careful  observation,  and  the  heart  examined  every  two 
or  three  days  for  some  weeks.  Any  exposure  to  chill 
should  be  guarded  against,  and  exercise  should  be  limited 
in  amount  for  some  time  after  all  apparent  symptoms  have 
subsided. 


44  HEART  DISEASE. 

Effusion. — If  extensive  effusion  into  the  pericardial  sac 
takes  place,  its  removal  by  paracentesis  may  be  necessary, 
and  it  is  important  that  this  should  not  be  long  delayed,  as 
death  from  syncope  is  liable  to  occur  from  embarrassment 
of  the  heart  by  the  pressure  of  the  fluid.  It  is,  however, 
frequently  a  difficult  matter  to  determine  whether  the 
symptoms  of  cardiac  embarrassment  and  the  increase  of 
cardiac  dulness  are  due  to  cardiac  dilatation  or  to  the 
presence  of  effusion,  and  not  infrequently  the  right  ventricle 
has  been  punctured  by  mistake.  I  have  seen  two  such 
cases  in  which  blood  was  withdrawn  from  the  right  ventricle 
but  no  ill  results  followed.  I  have,  however,  known  of 
two  cases  in  which  death  from  haemorrhage  resulted  from 
a  similar  procedure  where  cardiac  dilatation  was  mistaken 
for  effusion.  The  best  site  for  puncture  when  aspiration  is 
decided  on,  is  in  the  fifth  left  intercostal  space,  about  one 
inch  or  one  and  a  half  inch  external  to  the  border  of  the 
sternum,  outside  the  course  of  the  internal  mammary 
artery.  Some  advocate  that  this  puncture  should  be 
made  in  the  angle  between  the  xiphoid  cartilage  and  the 
costal  margin,  as  this  would  penetrate  the  lowest  part  of  the 
sac.  A  small  aspirating  needle  should  be  used,  and  previous 
to  its  insertion,  an  incision  should  be  made  down  through 
the  skin  to  the  intercostal  muscles.  Any  bulging  of  the 
intercostal  space  can  then  be  seen,  and  any  risk  of  wounding 
the  intercostal  arteries  be  avoided  by  keeping  close  to  the 
upper  border  of  the  rib. 

The  above  description  applies  to  the  type  of  pericar- 
ditis which  is  met  with  in  association  with  rheumatism  or 
pneumonia,  and  it  will  be  necessary  here  to  briefly  allude 
to  the  form  it  may  assume  in  Bright 's  disease. 

In  Bright 's  disease  pericarditis  occurs  most  commonly  as 
a  complication  of  subacute  parenchymatous  nephritis  or  of 
the  chronic  interstitial  variety.  Statistics  vary  as  to  its  fre- 
quency, from  3  to  14  per  cent.,  according  to  different  authors. 


ADHERENT  PERICARDIUM.  45 

The  onset  of  pericarditis  in  Bright's  disease  occurring, 
as  it  usually  does,  m  debilitated  subjects,  may  be  insidious 
and  unattended  by  any  marked  symptoms  of  local  reaction. 

There  may  be  little  or  no  rise  of  temperature,  no  pre- 
cordial pain,  and  little  beyond  increase  in  the  pulse-rate 
and  slight  exacerbation  of  pre-existing  systems,  such  as 
dyspnoea  and  restlessness  due  to  uraemia,  to  call  attention 
to  its  presence.  A  friction  rub  is  usually  present  and  is 
well  marked.  A  pleuritic  friction  rub  may  accompany  it, 
and  in  some  cases  a  pleuro-pericardial  rub  alone  is  heard, 
between  which  and  a  true  pericardial  rub  it  may  be  diffi- 
cult to  distinguish.  The  prognosis  is  always  very  grave  and 
the  treatment  must  be  directed  to  the  primary  disease. 

It  is  important,  therefore,  that  the  heart  should  be 
examined  as  a  matter  of  routine,  or  the  onset  of  peri- 
carditis may  easily  escape  notice. 


ADHEBENT  PEBICABDIUM. 

By  the  term  "adherent  pericardium"  is  implied  the  exist- 
ence of  adhesions  between  the  visceral  and  parietal  layers 
of  the  pericardium,  the  result  of  pericarditis. 

Morbid  Anatomy. — The  adhesions  may  be  limited  to  fibrous  bands 
stretching  across  the  pericardial  cavity,  or  they  may  be  universal,  in 
which  case  the  pericardium  and  heart  are  so  intimately  connected 
that  the  pericardial  cavity  is  entirely  obliterated.  Adhesions  may 
also  exist  between  the  chest-wall  or  pleura  and  the  pericardium,  as 
a  result  of  so-called  mediastino-pericarditis.  The  adhesions  if  of  old 
standing  are  tough  and  fibrous,  so  that  the  pericardium  cannot  be 
stripped  from  the  heart  without  tearing  the  heart-substance.  There 
is  also  commonly  some  fibroid  change  in  the  heart- wall  due  to  sub- 
stitution of  fibrous  tissue  for  muscle  fibres  damaged  by  previous 
inflammation.  In  the  case  of  recent  adhesions  or  lymph  undergoing 
organization  into  fibrous  tissue,  the  two  layers  of  pericardium  on 
being  separated  will  present  a  honeycomb  or  bread-and-butter-like 
appearance,  owing  to  the  layer  of  thick,  sticky  lymph  which  coats 
the  surface. 


46  heart  disease. 

Physical    Signs. 

The  physical  signs  differ  according  as  the  adhesions 
exist  only  between  the  two  layers  of  the  pericardium,  or 
between  the  pericardium  and  chest-wall,  or  adjoining 
pleura  as  well.  In  the  latter  case  they  are  more  numerous 
and  distinctive.     Among  them  are  the  following : — 

Fixation  of  the  apex  beat,  so  that  it  does  not  alter  its 
position  in  deep  inspiration  and  expiration  or  in  change 
of  posture  of  the  body. 

Systolic  depression  of  one  or  more  intercostal  spaces  to 
the  left  of  the  sternum,  or  of  the  lower  end  of  the  sternum 
and  the  adjoining  costal  cartilages,  which  may  be  caused 
by  the  heart  dragging  on  them  at  each  systole,  through 
the  agency  of  the  pericardial  adhesions.  The  systolic 
recession  of  spaces  alone  is,  however,  not  a  trustworthy 
indication,  as  it  may  be  due  to  atmospheric  pressure,  more 
especially  when  the  heart  is  much  hypertrophied.  When  the 
costal  cartilages  or  lower  end  of  the  sternum  are  dragged 
in  there  can  be  little  doubt  as  to  the  diagnosis,  as  this  could 
not  be  effected  by  atmospheric  pressure. 

Systolic  recession  of  the  site  of  the  apex  beat  is  an 
important  sign  when  a  definite  apex  beat  can  be  felt ; 
when  there  is  no  palpable  apex  beat,  systolic  pitting  over 
its  site  may  be  due  to  atmospheric  pressure. 

A  diastolic  shock  may  sometimes  be  felt  on  palpation 
with  the  flat  of  the  hand  over  areas  on  the  chest-wall  where 
systolic  recession  is  present.  It  is  due  to  the  elastic  recoil 
of  the  chest-wall  at  the  commencement  of  diastole  as  soon 
as  the  pulling  force  exerted  during  the  systole  ceases. 

Systolic  retraction  of  the  lower  portions  of  the  posterior 
or  lateral  walls  of  the  thorax  may  indicate  the  presence 
of  a  universally  adherent  pericardium.  Such  retraction 
may,  however,  be  seen  though  the  pericardium  is  not 
adherent  to  the  heart,  but  only  to  a  larger  extent    than 


ADHERENT  PERICARDIUM.  47 

normal  to  the  central  tendon  of  the  diaphragm  and  the 
muscular  substance  on  either  side,  and  to  the  chest-wall  as 
well.  In  such  cases  the  heart  is  usually  greatly  enlarged  and 
hypertrophied  from  old  valvular  disease.  The  explanation 
seems  to  be  that  the  portion  of  the  diaphragm  to  which 
the  pericardium  is  adherent  is  dragged  upwards  at  each 
systole  of  the  heart,  so  that  the  points  of  attachment  of 
the  digitations  of  the  diaphragm  to  the  lower  ribs  and 
costal  cartilages  are  dragged  inwards  and  retracted. 

The  descent  of  the  diaphragm  in  inspiration  may  be  inter- 
fered with  by  pericardial  adhesions  between  the  heart  and 
diaphragm,  more  especially  if  the  pericardium  is  adherent 
to  the  chest-wall  in  front  as  well.  This  will  be  shown  by 
impaired  movement  in  respiration  of  the  upper  part  of  the 
abdominal  wall  in  the  epigastrium  and  left  subcostal  region. 
The  area  of  cardiac  dulness  will  be  increased,  and  will 
remain  unchanged  in  inspiration  and  expiration,  where 
there  are  extensive  adhesions  between  the  pericardium  and 
chest- wall,  as  the  lung,  which  normally  overlaps  part  of 
the  heart,  will  have  been  pushed  aside,  or  perhaps  have 
become  involved  in  the  adhesions,  and  be  collapsed. 

Enlargement  of  Heart. — It  is  common  with  adherent 
pericardium  to  find  the  heart,  more  especially  the  right 
ventricle,  considerably  enlarged,  in  the  absence  of  valvular 
disease  or  other  obvious  cause  to  account  for  it. 

It  seems  probable  that  such  enlargement  may  be 
indirectly  due  to  pericardial  adhesions  as  follows :  The 
heart  becomes  dilated  during  an  attack  of  pericarditis, 
and,  before  it  recovers  its  tone  or  can  contract  down 
again  to  its  normal  size,  the  pericardium  becomes  adherent 
and  fixes  it  in  this  condition  of  dilatation,  the  right 
ventricle  suffering  more  than  the  left,  owing  to  its  thinner 
walls,  as  well  as  for  other  reasons. 

Hypertrophy  and  dilatation  of  the  heart,  more  especially 
of  the   right  ventricle,  may  therefore,  in  the   absence   of 


48  HEART  DISEASE. 

other  obvious  causes,  such  as  valvular  disease,  high  arterial 
tension,  etc.,  to  explain  it,  be  a  physical  sign  of  consider- 
able importance. 

Diastolic  collapse  of  cervical  veins  was  held  by  Friedreich 
to  be. of  great  diagnostic  value  when  accompanied  by  systolic 
retraction  of  spaces;  but  I  have  never  found  it  to  be  of  service. 

Systolic  emptying  of  veins  on  the  surface  of  the  thorax 
may  sometimes  be  observed,  due  to  suction  action,  in- 
duced by  the  walls  of  the  internal  mammary  veins  being 
dragged  apart  by  pericardial  adhesions  during  systole  of 
the  heart. 

When  there  are  no  adhesions  between  the  pericardium 
and  chest-wall  the  physical  signs  that  may  be  present 
will  be  limited  in  number.  There  will  be  no  recession  of 
spaces  except  as  the  result  of  atmospheric  pressure,  no 
fixation  of  apex  beat,  no  diastolic  shock.  As  the  pericardium 
is  normally  attached  by  fibrous  bands  to  the  central  tendon 
of  the  diaphragm  and  to  the  muscular  substance  on  either 
side  of  it,  there  may  be  some  interference  with  the  move- 
ments of  the  diaphragm  in  respiration.  There  may  also 
be  considerable  enlargement  of  the  heart,  but  in  these 
cases  a  diagnosis  will  usually  have  to  be  made  from  other 
indications  than  physical  signs  alone. 

Symptoms. — The  symptoms  in  themselves  are  not  in  any 
sense  characteristic.  They  are  usually  such  as  arise  from 
cardiac  embarrassment,  more  especially  from  the  giving  way 
of  the  right  ventricle,  such  as  oedeina  of  the  extremities, 
enlargement  of  liver,  ascites,  dyspnoea,  etc. 

Diagnosis. 

The  physical  signs  or  symptoms  of  adherent  pericardium, 
few  of  which  may  be  present,  are  often  in  themselves 
insufficient  to  allow  of  a  diagnosis  being  made,  or  even  to 
arouse  suspicion  of  its  presence ;  but  valuable  help  may  be 
derived  from  careful  consideration  of  the  physical  signs  and 


ADHERENT  PERICARDIUM.  49 

symptoms  together,  and  by  balancing  the  former  against 
the  latter,  so  that  the  question  is  raised,  "Do  the  physical 
signs  present  afford  evidence  of  sufficient  disease  to  account 
for  the  symptoms  that  have  arisen?"  When  the  symp- 
toms are  those  of  right  ventricle  failure,  and  are  more 
severe  than  the  physical  signs  present  would  lead  one  to 
expect,  and  have  not  been  induced  by  undue  exertion  or 
imprudence,  adherent  pericardium  must  be  thought  of  as 
being  possibly  responsible.  For  it  is  the  right  side  of 
the  heart  more  especially  that  is  seriously  hampered  by 
pericardial  adhesions,  so  that  their  presence  may  account 
for  the  unexpected  breakdown  of  the  right  ventricle  when 
the  physical  signs  indicate  that  the  valvular  lesion  is 
slight.  It  must  also  be  borne  in  mind  that  the  heart-wall 
has  in  all  probability  been  weakened  by  the  substitution 
of  fibrous  tissue  for  muscle  fibres  destroyed  by  inflammation 
at  the  time  of  the  attack  of  pericarditis. 

When  with  symptoms  of  right  ventricle  failure  there  is 
an  absence  of  cyanosis,  or  of  pulmonary  congestion  or  lung 
mischief,  this  is  further  evidence  in  favour  of  adherent 
pericardium  as  a  possible  cause  of  the  breakdown  of  the 
right  ventricle.  If  by  these  means  a  suspicion  of  the 
presence  of  adherent  pericardium  has  been  aroused,  con- 
firmatory physical  signs  should  be  carefully  sought  for. 

The  above  remarks  apply  to  the  question  of  diagnosis 
in  cases  where,  with  or  without  valvular  disease,  there  is  no 
history  of  pericarditis,  and  the  adhesions  are  of  old  standing. 

In  cases  of  pericarditis,  which  can  be  kept  under 
observation  after  the  attack,  there  will  be  less  difficulty  in 
arriving  at  a  diagnosis,  and  the  indications  which  would 
lead  one  to  suspect  that  the  pericardium  was  becoming- 
adherent  are  as  follows  : — 

1.  Prolongation  of  the  attack  of  pericarditis  evidenced 
by  a  harsh  friction  rub  over  the  precordial  area,  which  may 
persist  for  some  weeks.     When  at  the  margins  of  the  area  of 

E 


50  HEART  DISEASE. 

cardiac  dulness  a  pleuro-pericardial  friction  is  also  heard,  it 
will  indicate  that  adhesions  are  probably  taking  place  between 
the  pericardium  and  adjoining  pleura  or  chest-wall  as  well. 

2.  Permanent  enlargement  of  the  area  of  cardiac  dulness 
to  a  marked  extent  after  the  subsidence  of  the  pericarditis. 

3.  The  occurrence  of  symptoms  of  right  ventricle  failure 
after  a  period  of  temporary  improvement,  there  being  no 
apparent  exciting  cause  for  the  breakdown  of  the  right  ven- 
tricle. Damage  to  the  cardiac  muscle  by  fresh  myocarditis 
may,  however,  be  responsible,  and  should  be  first  excluded. 

Prognosis. 

When  the  heart  remains  normal  in  size,  and  there  are 
no  adhesions  between  the  pericardium  and  chest-wall,  the 
universal  adherence  of  the  pericardium  to  the  heart  may 
not  in  an  adult  tend  to  materially  shorten  life.  When 
the  heart  is  enlarged,  or  when  the  pericardium  is  also 
adherent  to  the  chest-wall,  the  prognosis  is  more  serious. 
When  adherent  pericardium  exists  as  a  complication  of 
valvular  disease,  it  is  still  more  likely  to  prove  fatal 
eventually,  by  so  hampering  the  right  ventricle  as  to 
prevent  its  recovery  when  once  compensation  has  broken 
down.  The  detection  of  adherent  pericardium  has  also  an 
important  bearing  on  prognosis,  inasmuch  as  it  affords  pre- 
sumptive evidence  of  fibroid  change  in  the  heart- wall,  and 
therefore  renders  the  outlook  even  more  unfavourable. 

Treatment. 

The  discovery  of  adherent  pericardium,  when  present,  is 
important  from  the  point  of  view  of  treatment,  not  because 
anything  can  be  done  to  remedy  or  remove  the  pericardial 
adhesions,  once  they  are  formed,  but  because,  when  it  is 
present,  it  will  be  necessary  to  impose  additional  restrictions 
on  the  patient,  so  that  no  undue  risks  may  be  run  of 
upsetting  the  compensatory  balance,  which  would  only  be 
restored  with  great  difficulty. 


SUPPURATIVE  PERICARDITIS.  51 


SUPPURATIVE   PERICARDITIS. 

Purulent  pericarditis  may  occur  as  part  of  a  general 
pyasrnic  or  septicemic  condition,  or  in  association  with 
einpysenia  or  some  pneumococcal  infection,  abscess  of  the 
lung,  suppuration  of  mediastinal  or  cervical  glands,  or  of 
other  adjacent  structures.  Sometimes  no  apparent  cause 
can  be  found. 

The  inflammatory  process  is  almost  invariably  septic  from 
the  onset,  and  is  attended  by  effusion  of  pus  into  the  peri- 
cardium :  seldom,  if  ever,  does  a  serous  effusion  of  rheumatic 
origin  become  purulent. 

The  outset  of  the  disease  is,  as  a  rule,  insidious,  and  the 
discovery  of  pus  in  the  pericardium  is  often  not  made  till 
the  post-mortem  examination. 

The  micro-organisms  which  have  been  found  are  the 
staphylococcus  pyogenes  aureus,  albus,  and  citreus,  the 
streptococcus,  and  the  pneumococcus. 

Physical  Signs. — There  is  seldom  any  definite  friction  rub 
to  announce  the  onset  of  the  attack. 

The  physical  signs  present  will  be  those  of  pericardial 
effusion,  which  have  already  been  discussed.  Chief  of  these 
is  increase  in  the  area  of  cardiac  dulness,  and  the  difficulty 
of  distinguishing  whether  this  be  clue  to  cardiac  dilatation 
or  effusion  will  be  intensified  when  no  friction  rub  has  been 
heard  to  suggest  the  possibility  of  effusion.  Furthermore, 
it  not  infrequently  happens  that  the  area  of  cardiac  dulness 
is  encroached  upon  by,  or  runs  into,  a  large  dull  area  due 
to  empysenia. 

Feebleness  or  loss  of  the  apex  beat,  and  weak  or  distant 
heart-sounds  may  be  noted,  but  will  not  be  of  great  value, 
unless  the  case  has  been  watched  from  the  outset,  so  that 
a  standard  of  comparison  could  be  formed.  There  may, 
occasionally,  be  oedema  over  the  precordial  region. 


52 


HEART  DISEASE. 


Symptoms. — The  temperature  is  usually  that  character- 
istic of  some  septic  infection,  but  may  sometimes  be  normal 
throughout.  Eigors  seldom  occur  unless  as  part  of  a  general 
septicaemia,  except  in  the  somewhat  rare  event  of  a  serous 
pericardial  effusion  becoming  purulent.  Pain  is  absent,  as 
a  rule,  but  there  may  be  a  feeling  of  oppression  in  the 
precordial  region.  The  pulse  rate  and  respiration  are 
accelerated,  and  there  may  be  marked  dyspnoea,  especially 
on  movement. 

Diagnosis. — The  diagnosis  presents  many  difficulties,  and 
is  frequently  not  made  during  life. 

In  the  absence  of  an  antecedent  friction  rub  effusion 
may  not  be  suspected,  and  the  intermittent  pyrexia  may  be 
attributed  to  an  empyaema,  or  suppuration  elsewhere  than 
in  the  pericardium. 

If  effusion  is  suspected,  an  exploring- needle  may  be 
employed.  The  skin  should  be  incised  parallel  to  the  ribs, 
as  described  under  paracentesis  pericardii,  and  the  intercostal 
muscles  divided  before  the  needle  is  inserted  into  the  peri- 
cardium, so  that  any  bulging  of  the  space  may  be  noted,  and 
the  needle  be  accurately  directed. 

Prognosis. — The  prognosis  is  always  very  serious,  but 
there  are  reasonable  grounds  for  hope  in  cases  where  the 
suppuration  is  not  part  of  a  general  septic  infection,  but 
is  a  sequela  of  an  empyema  or  other  localized  abscess. 

The  earlier  the  diagnosis  is  made  and  surgical  inter- 
ference is  sought,  the  better  will  be  the  chance  of  recovery. 
The  percentage  of  recoveries  is,  however,  very  small. 

Treatment. — Abscess  in  the  pericardium  must  be  treated 
like  any  other  abscess.  It  should  be  opened  and  drained  as 
soon  as  the  diagnosis  is  made,  by  an  incision  in  the  fifth 
space,  close  to  the  sternum  on  the  right  or  left  side,  wherein 
any  bulging  of  the  intercostal  space  is  apparent, 

Hydropericardium. — By     hydropericardimn     is     meant 
effusion  of  serous   fluid   into   the   pericardial    sac,  as  the 


SUPPURATIVE  PERICARDITIS.  53 

result,  not  of  inflammation,  but  of  passive  dropsical  trans- 
udation. 

Effusion  of  such  degree,  as  to  be  clinically  recognizable, 
occurs  most  commonly  as  part  of  a  general  dropsical  trans- 
udation from  whatever  cause,  and  is  therefore  most  frequently 
associated  with  Bright's  disease  or  morbus  cordis.  It  is  much 
less  common  than  effusion  into  other  serous  cavities,  and 
when  present  is  a  late  feature  in  the  disease,  and  is  gradual 
in  onset.  It  is  said  also  to  occur  as  the  result  of  mechanical 
obstruction,  to  the  return  of  blood  from  the  pericardial 
and  cardiac  veins  from  some  local  cause,  such  as  pressure 
by  mediastinal  tumours,  enlarged  glands,  or  fibrous 
adhesions,  but  this  must  be  very  exceptional. 

Symptoms  and  Physical  Signs  and  Diagnosis. — The 
symptoms  are  increasing  dyspncea  and  precordial  oppres- 
sion with  enfeeblement  of  the  pulse,  and  the  physical  signs 
are  those  of  pericardial  effusion,  increase  of  the  area  of 
cardiac  dulness,  with  progressive  enfeeblement  of  the  apex 
beat  and  weakness  of  the  heart-sounds.  As  there  is  no 
antecedent  friction  rub  to  call  attention  to  the  possibility 
of  effusion,  it  may  readily  escape  notice  in  the  earlier  stages. 
The  diagnosis  cannot  be  made  unless  the  effusion  amounts 
to  several  ounces,  and  when  there  is  effusion  into  one  or 
both  pleural  cavities  as  well  it  is  very  difficult,  and  may  be 
impossible. 

Treatment. — Practically  the  treatment  is  that  of  the 
original  disease  to  which  the  general  dropsy  and  hydro- 
pericardium  are  due.  Belief  may  occasionally  be  afforded 
by  aspiration  of  the  pericardium  when  the  diagnosis  of 
effusion  can  be  made  with  certainty ;  but  it  is  rarely  em- 
ployed or  called  for,  as  the  relief  can  but  be  temporary,  and 
does  not  long  delay  the  fatal  result. 

Pneumopericardium. — The  presence  of  gas  in  the  peri- 
cardial sac  is  rare.  It  may  be  due  to  penetrating  wounds 
of  the  pericardium  by  a  sharp  instrument  or  a  fractured  rib, 


54  HEART  DISEASE. 

but  is  more  commonly  the  result  of  ulceration,  Ly  which  a 
communication  is  established  between  the  pericardial  sac 
and  an  air-containing  cavity.  Thus,  an  old  phthisical  cavity, 
an  abscess  in  the  lung,  a  pneumothorax,  a  subphrenic  abscess 
that  has  made  its  way  through  the  diaphragm,  may  open 
into  the  pericardium,  or  a  communication  may  be  established 
with  the  oesophagus  by  ulceration,  giving  rise  in  each  in- 
stance to  pneumopericardium.  Pus  may  find  its  way  into 
the  pericardium  with  the  air  giving  rise  to  pyo-pneumo- 
pericardium,  or  blood  in  the  case  of  punctured  wounds,  when 
the  condition  is  termed  hasmo-pneuniopericardiuni. 

Physical  Signs. — Uniform  bulging  of  the  precordial  area 
may  be  noted.  The  apex  beat  is  usually  absent  or  feeble, 
but  can  sometimes  be  felt  when  the  patient  bends  forwards. 

On  percussion  the  note  varies  with  change  of  position, 
being  dull  over  the  fluid  and  tympanitic,  or  high  pitched 
over  the  air-containing  cavity.  The  gas  always  rises  to  the 
highest  part  of  the  cavity  with  change  of  posture  of  the 
patient.  The  relations  of  the  gas  and  fluid  will  be  remark- 
ably altered  by  changes  of  posture,  and  can  be  readily  made 
out  by  percussion. 

On  auscultation  the  heart-sounds  acquire  a  peculiar 
metallic  character,  and  are  unusually  loud  and  clear,  so  that 
they  may  sometimes  be  heard  at  some  distance  off,  and  are 
a  source  of  annoyance  to  the  patient  himself.  Splashing 
sounds,  and  metallic  tinkling,  and  a  bell  note  with  coins 
can  usually  be  heard. 

Treatment. — As  pneumopericardium  is  usually  a  com- 
plication of  some  grave  disease,  treatment  must  vary  accord- 
ingly. Aspiration  may  be  required  to  remove  the  gas  or 
fluid,  or  possibly  free  incision  may  be  necessary  to  allow 
of  the  escape  of  pus. 

Tuberculosis  of  the  pericardium  may  occur  as  part  of  a 
general  acute  miliary  tuberculosis,  when  miliary  tubercles 
will   be   found   scattered  over  its  surface,  post-mortem,  or 


SUPPURATIVE  PERICARDITIS.  55 

from  direct  infection  by  adjacent  tubercular  lung  or  pleura, 
in  which  case  the  onset  is  insidious  and  the  progress  of  the 
disease  is  usually  chronic.  The  two  layers  of  pericardium 
become  thickened  and  tend  to  become  adherent,  so  that 
the  physical  signs  are  those  of  chronic  mediastinitis,  or 
adherent  pericardium. 

New  growth  of  the  pericardium  is  very  rare,  and  when 
found  is  usually  due  to  invasion  of  the  pericardium  by  a 
new  growth  in  adjacent  structures. 


CHAPTEE  IV. 

SIMPLE    ACUTE   ENDOCARDITIS. 

Acute  endocarditis  means,  strictly  speaking,  an  acute 
inflammation  of  the  endocardium  or  lining  membrane  of 
the  heart.  The  inflammatory  process  is,  however,  as  a  rule, 
chiefly  manifested  on  the  valves,  so  that  by  the  term  endo- 
carditis is  usually  understood  inflammation  of  the  valves 
of  the  heart.  The  mitral  and  aortic  valves  are  most  com- 
monly attacked ;  rarely  are  the  valves  of  the  right  side 
of  the  heart  affected  except  as  a  result  of  endocarditis 
occurring  during  intra-uterine  life.  It  must  be  borne  in 
mind  that  acute  endocarditis  is  commonly  accompanied  by 
myocarditis  of  varying  extent,  which  may  seriously  and 
permanently  damage  the  walls  of  the  heart. 

On  etiological  and  pathological  grounds  it  is  doubtful 
whether  simple  or  rheumatic  endocarditis  should  be 
differentiated  from  malignant  or  pernicious  endocarditis, 
and  this  question  is  discussed  fully  in  the  chapter  on 
the  latter  affection.  Clinically,  the  two  diseases  are  more 
or  less  distinct,  and  for  that  reason  they  are  here  considered 
separately. 

Morbid  Anatomy  and  Pathology. — On  naked-eye  exami- 
nation of  an  affected  valve  it  is  seen  to  be  studded  along 
the  free  margin  with  small  greyish-yellow  or  pinkish  opaque 
bodies,  the  so-called  "  vegetations,"  as  shown  on  the  aortic 
valves  in  Fig.  7.  Microscopically  these  are  seen  to  consist 
of  a  superficial  layer  of  coagulated  fibrin  and  necrotic  tissue, 
in  the  upper  stratum   of  which  are   entangled  leucocytes 


SIMPLE  ACUTE  ENDOCARDITIS. 


57 


and  a  few  red  corpuscles  deposited  from  the  blood  stream. 
Deeper  down  is  a  layer  of  simple  fibrin  free  from  corpus- 
cular elements,  and  below  this,  again,  is  a  layer  of  granula- 
tion tissue,  formed  by  proliferation  of  the  endothelial  cells 


as  a  result  of  the  inflammatory  process.  The  inappropriately 
named  "  vegetations "  are  thus  simply  necrotic  tissue, 
coagulated  fibrin  and  leucocytes  deposited  from  the  blood 
stream  on  an  inflamed  surface.  They  may  become  partially 
absorbed,  but,   for  the   most  part,  the   granulation   tissue 


58  HEART  DISEASE. 

undergoes  organization,  and,  later  on,  cicatricial  con- 
traction, so  that  the  valves  become  puckered  and  mis- 
shapen,  sometimes  glued  together  at  their  margins,  and 
incompetence  or  obstruction,  or  both  combined,  result. 
When  the  mitral  valve  is  affected,  the  chordae  tendinese 
are  also,  as  a  rule,  more  or  less  involved  in  the  inflam- 
matory process,  so  that  they  become  shortened,  thickened 
and  deformed,  and  lose  their  flexibility.  The  shortening 
and  fusing  together  of  their  fine  subdivisions  near  the  valves 
may  be  carried  to  such  an  extent  that  the  margins  of  the 
valves  seem  to  be  directly  attached  to  the  papillary  muscles. 

Etiology. — Acute  endocarditis  is  in  the  great  majority 
of  cases  a  complication,  or  rather  an  essential  feature  of 
rheumatism. 

Of  late  years  much  evidence  has  been  accumulated 
tending  to  prove  that  rheumatism  is  a  disease  of  microbic 
origin,  and  that  the  valvulitis  associated  with  it  is  a  local 
manifestation  of  the  activity  of  specific  micro-organisms. 
The  micro-organism  in  question  is  a  minute  diplococcus 
which  has  been  isolated  from  the  blood  and  pericardial  fluid 
of  patients  suffering  from  acute  rheumatism  by  various 
observers,  Triboulet,*  Wasserman,f  Paine  %  and  Poynton, 
Shaw,§  Ainley  Walker,  Beattie,  and  others.  This  diplo- 
coccus, grown  on  suitable  media  and  inoculated  into  rabbits, 
has  in  their  hands  produced  arthritis,  endocarditis,  and 
valvulitis,  and  in  early  cases  of  rheumatic  endocarditis 
minute  diplococci  can  sometimes  be  demonstrated  micro- 
scopically in  the  vegetations  on  the  affected  valves.  Acute 
endocarditis  occurring  in  association  with  chorea  may  be 
regarded  as  of  rheumatic  origin. 

It  is  not  uncommon  as  a  sequela  to  scarlet  fever. 
The  type  sometimes   met  with  in   smallpox,  measles,  and 

*  Bulletin  de  la  Soc.  des  hopitaux,  1898,  p.  93,  n. 
f  Berliner  Klin.  Woch.,  1899,  No.  29,  p.  638. 
X  Lancet,  Sept.  1900. 
§  Journal  Path,  and  Bad.,  Dec.  1903. 


SIMPLE   ACUTE  ENDOCARDITIS.  59 

pneumonia  belongs  rather  to  the  category  discussed  in  the 
next  chapter. 

Cole  *  has  succeeded  in  producing  valvulitis  and 
arthritis  in  rabbits  by  inoculating  them  with  different 
brands  of  streptococci  obtained  from  cases  of  puerperal 
fever,  septic  peritonitis,  and  other  sources,  in  which  there 
was  no  history  of  rheumatism,  the  results  being  similar 
to  those  obtained  by  Paine  and  Poynton,  Shaw,  etc.,  by 
inoculation  with  the  diplococcus  isolated  from  cases  of 
rheumatism.  He  therefore  argues  that  there  is  no  such 
thing  as  a  specific  rheumatic  micro-organism,  and  the 
question  is  still  to  a  certain  extent  sub  judice.  But,  in 
view  of  the  results  obtained  by  Paine  and  Poynton  and 
others,  it  scarcely  seems  fair  to  argue  that  because  micro- 
organisms other  than  those  associated  with  rheumatism  can 
produce  endocarditis  in  animals,  as  has  long  been  known  in 
the  case  of  man,  therefore  there  is  no  specific  rheumatic 
organism.  Moreover,  rheumatism,  whether  in  the  child  or 
adult,  is  such  a  definite  clinical  entity,  that  one  would 
expect  to  find  a  specific  organism,  and  would  be  confusing  to 
vaguely  classify  it  as  a  form  of  "  septicaemia  "  in  the  ordinary 
sense  of  the  term.  We  must  hope  that  further  work  will 
be  done  on  this  subject,  and  that  future  investigators  will 
be  able  to  definitely  settle  the  controversy. 

It  is  most  common  in  childhood  and  early  adolescence, 
and  is  rare  after  middle  age.  It  may  also  occur  during  foetal 
life,  when  it  is  usually  confined  to  the  right  side  of  the  heart. 

Physical  Signs. 

The  development  of  a  valvular  murmur,  or,  in  the  case 
of  a  second  attack,  of  some  change  in  the  character  of  an 
existing  murmur,  is  the  only  trustworthy  indication  of  the 
presence  of  endocarditis.  Evidence,  however,  of  its  exist- 
ence is  frequently  found   post-mortem   in  cases  where  no 

*  Journal  Infect.  Diseases,  vol.  i.,  No.  4,  pp.  714-737. 


60  HEART  DISEASE. 

murmur  has  been  audible  during  life,  so  that  it  is  prob- 
able that  in  many  instances  the  inflammatory  process  may 
be  active  for  some  little  time  before  a  murmur  is  developed. 
It  is  important,  therefore,  to  be  on  the  look-out  for  other 
indications  of  its  presence  which  may  precede  the  develop- 
ment of  a  murmur,  however  indefinite  and  uncertain 
they  may  be.  Of  these  the  most  significant  is  some 
alteration  in  the  first  sound,  which  may  be  reduplicated, 
prolonged  and  muffled,  or  rumbling  in  character,  when  the 
mitral  valve  is  affected.  The  action  of  the  heart  may  be 
tumultuous  or  irregular,  and  the  area  of  cardiac  dulness  may 
become  much  enlarged,  when  the  inflammatory  process 
involves  the  muscular  substance  of  the  heart  as  well. 

These  indefinite  signs  are  chiefly  of  value  when  present  in 
cases  in  which  an  attack  of  endocarditis  is  to  be  anticipated, 
and  it  is  therefore  necessary  that  we  should  recognize  such 
cases  at  the  earliest  possible  moment.  Of  course,  in  a  well- 
marked  attack  of  rheumatism  of  the  usual  type  in  adults,  we 
shall  be  on  our  guard  ;  but  in  children,  as  pointed  out  by 
Cheadle,*  the  articular  manifestations  are  usually  slight, 
and  may  be  confined  to  fugitive  pains  in  the  joints,  while 
the  heart  is  frequently  attacked.  The  symptoms  of 
rheumatism  may  thus  be  so  ill-defined  as  to  escape  notice, 
and  the  onset  of  endocarditis  may  be  very  insidious. 

To  give  an  illustration  of  a  case  in  point.  Patrick  D., 
aet.  14,  employed  at  one  of  the  large  shops  in  London, 
walked  up  to  the  out-patient  department  at  St.  Mary's 
Hospital  on  2nd  January,  1897.  He  stated  that  he  had 
vomited  the  previous  day  after  having  some  pork  for 
dinner,  and  complained  of  being  rather  short  of  breath.  It 
was  noticed  that  he  was  somewhat  cyanosed,  and  was 
breathing  rapidly,  and  the  pulse  rate  was  132.  On 
examining  his  chest,  well-marked  pulsation  in  the  epigas- 
trium, and  in  the  third,  fourth,  and  fifth  left  intercostal 
*  Harveian  Lectures,  3889. 


SIMPLE  ACUTE  ENDOCARDITIS.  61 

spaces,  was  noted.  The  apex  beat  was  diffuse,  and  was 
visible  in  the  fifth  left  space  just  outside  the  vertical  nipple 
line.  The  area  of  cardiac  dulness  was  enlarged  and 
extended  to  the  right,  half  an  inch  beyond  the  right  border 
of  the  sternum ;  to  the  left,  just  beyond  the  vertical  nipple 
line;  and  above,  to  the  third  space.  At  the  apex  a  loud 
blowing  systolic  murmur  was  heard,  conducted  into  the 
axilla,  and  at  the  base,  over  the  aortic  area,  a  soft  diastolic 
murmur  conducted  down  the  sternum.  There  was  no  marked 
throbbing  of  the  carotids,  the  pulse  was  not  collapsing  in 
character,  and  a  distinct  aortic  second  sound  was  audible  at 
the  base  as  well  as  the  diastolic  murmur;  the  pulmonic 
second  sound  was  accentuated.  The  liver  was  somewhat 
enlarged,  but  there  was  no  oedema  of  the  extremities. 
Rheumatic  nodules  were  present  on  the  elbows  and  knees. 

The  history  given  by  the  boy  was  that,  two  months  ago 
he  had  felt  some  stiffness  in  the  knees,  and  had  remained  at 
home  two  days.  He  soon  felt  all  right  again,  and  up  to 
the  day  on  which  he  came  up  to  the  hospital  he  had  been 
at  work  as  usual.  He  was  at  once  admitted,  but  got  rapidly 
worse,  suffering  from  great  dyspnoea,  and  repeated  attacks 
of  vomiting  ;  the  diastolic  murmur  became  more  pronounced, 
and  the  pulse  collapsing  in  character ;  the  cardiac  dilatation 
increased  :  the  liver  became  more  and  more  enlarged,  and 
oedema  of  the  lower  extremities  set  in,  and  soon  became 
extreme.  He  died  on  17th  February,  six  and  a  half  weeks 
from  the  date  of  his  admission. 

The  stiffness  in  the  knees,  two  months  before  he  came 
up  to  the  hospital,  seems  to  have  been  the  only  warning  of 
the  attack  of  rheumatism  which  gave  rise  to  such  serious 
cardiac  mischief ;  and  so  slight  were  the  symptoms,  that 
the  boy  was  undoubtedly  going  about  his  work  with  active 
endocarditis  and  myocarditis  for  some  time  before  he  sought 
medical  advice,  and  by  that  time  the  heart  had  become 
dilated   to  an   extreme  decree.      This  case  illustrates  the 


62  HEART  DISEASE. 

insidious  form  that  the  rheumatism  of  early  adolescence  or 
childhood  may  assume,  and  shows  how  much  damage  may 
be  done  to  the  heart  before  any  serious  symptoms  compel 
the  patient  to  give  in. 

A  history  of  pains  in  the  joints  or  limbs,  with  slight 
febrile  disturbance  in  children,  should,  therefore,  put  us  on 
our  guard,  even  though  there  be  no  appreciable  swelling  or 
tenderness  of  the  joints,  and  the  heart  should  be  examined, 
not  only  when  the  patient  is  first  seen,  but  from  time  to 
time  for  some  weeks  afterwards.  A  family  history  of 
rheumatism,  or  of  a  previous  attack  of  chorea,  should  make 
us  doubly  suspicious  of  these  ill-marked  symptoms. 

There  are,  however,  certain  unmistakable  danger-signals 
for  which  we  should  be  on  the  look-out,  in  children  or 
young  adolescents,  when  a  suspicion  of  rheumatism  is 
aroused.  These  are  rheumatic  nodules — small  fibrous 
growths,  commonly  about  the  size  of  a  split  pea,  some- 
times much  larger.  They  are  found  in  the  neighbourhood 
of  joints  over  the  bony  prominences,  and  are  attached  by 
their  base  to  the  fascia,  sheaths  of  tendons,  or  some  under- 
lying fibrous  tissue.  The  skin  over  them  is  freely  movable, 
and  they  are  best  seen  by  flexing  the  joint  over  which 
they  are  situated,  so  that  the  skin  is  rendered  tense. 
They  were  first  described  by  Barlow  *  and  Warner ;  and 
Cheadle,  in  his  book  on  the  rheumatic  state  in  children, 
has  called  attention  to  their  evil  prognostic  significance. 
In  themselves  they  are  painless,  and  cause  little  or  no 
discomfort  to  the  patient,  but  they  indicate  that  the 
rheumatism,  to  which  they  owe  their  existence,  has  got  a 
firm  hold  on  its  victim,  and  where  they  are  present  in 
force,  repeated  attacks  of  cardiac  inflammation  are  to  be 
apprehended,  though  cases  do  occur  in  which  the  heart 
escapes.  They  are  not  present  in  all,  or  in  the  greater  pro- 
portion of  cases  in  which  the  heart  is  attacked,  but  a  careful 

*  Tram.  Internal.  Med.  Congress.    Londou,  1SS1. 


SIMPLE  ACUTE  ENDOCARDITIS.  63 

search  for  them  should  never  be  omitted,  as  they  are  of 
great  clinical  importance.    They  are  seldom  found  in  adults. 

Exudative  erythcmata,  of  the  type  of  erythema  margi- 
natum, or  less  commonly  papular  or  urticarial  in  character, 
may  occur  in  rheumatic  subjects ;  they  are  not  so  frequently 
met  with  as  nodules,  but  they  may  occur  in  conjunction 
with  them,  or  alone. 

In  erythema  marginatum,  small  raised  patches  about 
the  size  of  a  sixpence,  with  sharply  defined  margins,  and 
of  a  dull  red  colour,  make  their  appearance.  The  centre  of 
the  patch  usually  undergoes  absorption,  and  becomes  of  a 
pinkish  or  pale  colour,  while  the  margins  continue  to  spread 
as  narrow  raised  red  bands  with  irregular  outline.  The 
eruption  is  usually  accompanied  by  some  rise  of  tempera- 
ture, and  lasts  a  few  days,  gradually  fading  and  leaving  a 
slight  brownish  discoloration. 

Erythema  nodosum  is  sometimes  looked  upon  as  evidence 
of  rheumatism,  but  it  is  by  no  means  certain  that  it  can  be 
regarded  as  such. 

Symptoms. 
The  symptoms  are  not  specially  characteristic,  and  are, 
to  a  great  extent,  merged  in  those  of  the  rheumatic  affection 
of  which  endocarditis  is  a  part.  Dyspncea,  a  tendency  to 
sigh,  a  feeling  of  oppression  in  the  precordial  region,  rest- 
lessness, prolonged  fever  (the  temperature  not  ranging  high, 
as  a  rule,  but  from  99°  to  101°  F.),  a  fresh  rise  of  tempera- 
ture after  a  period  of  quiescence,  increase  of  the  pulse  rate, 
are  all  symptoms  which  may  give  rise  to  a  suspicion  of 
endocarditis,  and  be  present  during  an  attack  ;  but  reliance 
cannot  be  placed  on  these  alone  for  purposes  of  diagnosis. 

Pkognosis. 

During  an  attack  of  endocarditis,  it  is  practically  im- 
possible to  determine   exactly  the   extent  of  the  damage 


64  HEART  DISEASE. 

done  to  the  valves  attacked.  It  is  not  till  some  time  after 
the  inflammatory  process  has  subsided  and  compensatory 
changes  have  in  some  degree  developed,  that  we  are  able 
to  estimate  the  extent  of  the  lesion.  If,  in  the  course  of 
an  attack,  a  diastolic  murmur  develops  over  the  aortic  area, 
we  may  be  certain  that  the  aortic  valves  have  been  damaged, 
and  a  certain  degree  of  aortic  incompetence  will  perma- 
nently result.  It  does  not,  however,  in  the  case  of  the 
mitral  valve,  necessarily  follow,  when  a  systolic  murmur  is 
developed  at  the  apex,  that  the  mitral  incompetence  which 
the  murmur  indicates  will  be  permanent,  though  this  may 
be  the  case.  For  the  contractile  ring  surrounding  the 
mitral  orifice,  and  the  musculi  papillares  may  be  tempo- 
rarily thrown  out  of  gear  by  the  inflammatory  process,  so 
that  the  valves,  though  undamaged,  do  not  come  together 
at  their  margins,  and  some  regurgitation  takes  place,  or 
the  murmur  may  be  the  result  of  dilatation  of  the  ventricle. 
As  the  muscular  fibres  recover  their  tone  after  the 
inflammation  has  subsided,  the  valves  may  again  become 
competent,  and  the  systolic  murmur  disappear.  If,  how- 
ever, the  valves  themselves,  or  the  chordae  tendinese,  are 
seriously  attacked,  the  former  may  become  rigid  and 
deformed,  the  latter  puckered  and  shortened,  and  permanent 
incompetence  results. 

When  the  valves  become  thickened  and  glued  together 
at  their  margins,  stenosis  of  the  orifice  will  ensue,  which 
gradually  increases  as  cicatricial  contraction  of  the  freshly 
organized  fibrous  tissue  at  the  bases  of  the  valves  and  round 
the  mitral  orifice  takes  place.  Not  infrequently  incompe- 
tence and  stenosis  co-exist,  the  valves  being  thickened  and 
depressed  so  that  they  cannot  function  effectively,  while 
they  are  also  adherent  where  they  meet  at  their  attach- 
ment to  the  margin  of  the  orifice. 


simple  acute  endocarditis.  65 

Diagnosis. 

When  no  cardiac  murmur  is  present,  a  diagnosis  of 
endocarditis  is  not  possible.  It  is  not  always  easy  on 
discovering,  for  the  first  time,  the  existence  of  a  cardiac 
murmur,  to  decide  whether  or  not  it  indicates  acute  endo- 
carditis. It  may  be  due  to  a  recent  or  old  attack  of 
endocarditis,  to  cardiac  dilatation,  or  to  anseniia.  When 
hypertrophy  or  other  compensatory  changes  of  the  heart 
are  present,  they  will  testify  to  a  valvular  lesion  of  old 
standing,  but  in  such  cases  we  must  bear  in  mind  the 
possibility  and  probability  of  a  second  attack,  and  watch 
carefully  for  any  change  in  the  character  of  the  existing 
murmur,  or  for  the  development  of  a  new  murmur.  The 
history  of  the  case,  the  presence  of  nodules,  articular  pains, 
or  other  rheumatic  manifestations,  will  be  of  assistance 
in  arousing  suspicion  of  acute  endocarditis,  and  confirma- 
tory evidence  may  be  found  in  an  irregular  slightly  raised 
temperature,  or  restlessness  and  dyspnoea,  and  other 
symptoms  of  cardiac  disturbance.  The  murmurs  of  anaemia 
have  been  discussed  elsewhere  ;  the  history  of  the  case, 
the  aspect  of  the  patient,  and  the  character  of  the  murmur 
will  usually  enable  us  to  distinguish  these.  Exocardial 
murmurs,  whether  due  to  pericarditis  or  pleurisy,  are,  as  a 
rule,  readily  distinguished  by  their  harsh  grating  or  rubbing 
character,  their  position,  and  their  relation  to  the  cardiac 
rhythm. 

The  murmur  caused  by  compression  of  a  thin  layer  of 
lung  between  the  heart  and  chest  wall  may  be  excluded  by 
its  occurring  only  during  inspiration,  and  disappearing 
when  the  patient  is  told  to  make  a  deep  expiration  and  hold 
his  breath. 

Treatment. 

Neither  drugs  nor  local  applications  seem  to  be  of  avail 
to  arrest  the  progress  of  endocarditis,  or  modify  its  course 


66  HEART  DISEASE. 

in  an  appreciable  degree.  Salicylates,  alkalies,  iodides, 
quinine,  internally,  and  applications  over  the  prsecordial 
area  of  blisters,  sinapisms,  leeches,  and  ice-bags  have  been 
tried,  but  it  is  impossible  to  estimate  with  any  degree  of 
confidence  their  influence  on  the  inflammatory  process. 
Salicylates  and  salicin,  while  exercising  an  undoubted 
influence  on  the  rheumatic  condition,  have  no  effect 
on  the  inflammatory  process  as  such,  and  they  weaken 
the  heart  when  taken  continuously  for  any  considerable 
time.  Alkalies  are  less  open  to  objection,  especially  when 
given  with  quinine :  citrates  may  lessen  the  tendency  to 
deposition  of  fibrin  on  the  valves  by  diminishing  the 
coagulability  of  the  blood,  and  thus  perhaps  prove  of 
service.  We  shall  do  the  best  for  the  patient  by  keeping 
him  in  bed  and  treating  symptoms  as  they  arise,  giving 
only  an  effervescing  mixture  of  quinine  and  citrate  of 
potash.  At  any  rate,  no  active  measures  should  be  taken 
which  could  in  any  way  impair  his  strength  or  increase 
his  discomfort.  The  patient  should  be  kept  in  bed,  not 
only  during  the  attack,  but  for  some  weeks  or  months  after 
it  has  subsided,  till  sufficient  time  has  elapsed  for  the 
heart  to  recover,  and  for  compensatory  changes  to  take 
place.  In  children  who  come  of  a  rheumatic  stock,  a 
careful  look-out  must  be  kept  for  any  of  the  premonitory 
symptoms  of  rheumatism  or  heart  inflammation,  and  if 
any  suspicion  is  aroused  that  the  heart  is  being  attacked, 
the  child  should  be  kept  in  bed  till  all  doubt  is  over. 


CHAPTER   V. 

"MALIGNANT"   OR  "PERNICIOUS"  ENDO- 
CARDITIS. 

NOMENCLATURE  OF  THE  AFFECTION — MORBID  ANATOMY — 
ETIOLOGY— THE  ROLE  PLAYED  BY  VARIOUS  MICRO- 
ORGANISMS—PHYSICAL SIGNS  AND  SYMPTOMS— INFARC- 
TION AND  EMBOLISM — DIAGNOSIS — PROGNOSIS — TREAT- 
MENT.     CHRONIC   ENDOCARDITIS. 

To  this  form  of  endocarditis  various  epithets  have  been 
applied  to  distinguish  it  from  "  simple  or  rheumatic " 
endocarditis :  "  infective "  because  of  its  microbic  origin, 
"  malignant  "  because  of  its  fatal  tendency,  "  ulcerative  " 
because  of  the  severity  of  the  lesions  in  the  valves  attacked. 
In  view  of  recent  researches,  which  tend  to  prove  that 
rheumatism  is  a  disease  due  to  a  specific  micro-organism 
which  may  be  widely  distributed  in  the  body,  the  term 
"  infective  "  is  no  longer  appropriate,  nor  is  "  ulcerative  " 
specially  suitable,  as  ulceration  of  the  valves,  though 
frequent  and  extensive,  is  not  an  essential  characteristic. 
We  are  left,  then,  with  "  malignant,"  which,  though  not  a 
highly  scientific  effort,  may  be  truthfully  employed  as 
expressing  the  grave  nature  of  the  malady ;  but,  inasmuch 
as  recovery  undoubtedly  occurs  in  some  cases,  it  is  not 
employed  in  quite  the  same  sense  as  when  we  speak  of 
"malignant"  disease  as  a  synonym  for  carcinoma.  We 
would  venture  to  suggest  the  term  "  pernicious      as  a  more 


68  HEART  DISEASE. 

appropriate  epithet,  used  in  the  same  sense  as  in  "  pernicious 
anaemia,"  which,  while  it  denotes  the  serious  nature  of  the 
disease,  does  not  necessarily  connote  a  fatal  issue. 

It  is  indeed  difficult,  if  not  impossible,  to  draw  a  hard- 
and-fast  line  between  "simple  or  rheumatic"  and  "per- 
nicious "  endocarditis,  and,  as  will  be  seen  later  in  the 
section  on  etiology,  there  is  convincing  evidence  in  favour 
of  the  view  that  "  pernicious  "  endocarditis,  in  a  certain 
proportion  of  cases,  is  a  virulent  form  of  rheumatic  endo- 
carditis, and  due  to  the  same  micro-organism. 

Because  simple  endocarditis  is  not  a  fatal  malady,  we 
rarely  find  at  autopsies  the  small  bead-like  vegetations  on 
the  valves  supposed  to  be  characteristic  of  this  affection, 
unless  the  patient  has  succumbed  to  pericarditis  or  some 
intercurrent  malady.  But  in  children  it  is  a  common  ex- 
perience to  meet  with  repeated  and  prolonged  attacks  of 
endocarditis,  in  which  the  temperature  ranges  from  99  to  101 
degrees  for  some  weeks,  and  the  cardiac  murmur  changes 
in  character,  the  child  becoming  progressively  anseinic, 
but  eventually  recovering,  with  well-marked  signs  of  mitral 
incompetence.  Because  there  is  no  evidence  of  infarc- 
tion, and  the  temperature  is  not  high,  and  the  child  does 
not  succumb  at  the  time,  it  is  customary  to  classify  these 
as  cases  of  simple  rheumatic  endocarditis,  though  probably 
they  form  an  intermediate  group  between  the  two  extremes. 
Again,  when  we  meet  with  old  cicatrized  lesions  of  the 
valves,  such  as  the  "  button-hole  "  mitral  orifice,  or  great 
deformity  of  the  aortic  valves,  in  patients  who  succumb 
from  the  effects  of  these  chronic  valvular  lesions,  which 
from  their  very  appearance  must  have  been  due  to  extensive 
damage  and  ulceration  of  the  valves  which  have  healed  and 
cicatrized,  we  may  justly  infer  that  these  were  cases  of 
ulcerative  endocarditis  at  the  outset,  and  they  form  another 
link  in  the  chain  between  the  mild  and  fatal  varieties  of 
acute  endocarditis. 


"MALIGNANT"    OR    "PERNICIOUS"    ENDOCARDITIS     69 

Gibson,  in  his  treatise  on  the  Heart,  does  not  make  any 
distinction  in  nomenclature  between  the  various  grades,  but 
includes  all  varieties  under  the  term  "acute  endocarditis." 

It  is,  however,  convenient  for  clinical  purposes  to  dif- 
ferentiate two  main  groups,  as  we  have  done  here,  as  there 


FIG.    8.— DESTRUCTION   OF   PULMONIC   VALVES   BY   PERNICIOUS   ENDOCARDITIS, 
AND   VEGETATIONS   ON   THE   PULMONARY    ARTERY. 


are  certain  clinical  and  pathological  features  which  mark 
them  off  one  from  the  other. 

Morbid  Anatomy. — The  affected  valves  are  usually 
masked  by  large,  fungating  vegetations  readily  detachable 
and  extremely  friable.     On  removal  of  these  vegetations, 


7o  HEART  DISEASE. 

the  valve  is  frequently  found  to  be  partially  or  wholly 
destroyed  by  ulceration.  The  disease  is  often  not  limited 
to  the  valves,  and  vegetations  or  erosions  may  be  present  on 
the  endocardium  lining  the  cavities  of  the  heart,  especially 
the  auricles,  on  the  inner  surface  of  the  walls  of  the  great 
vessels,  as  in  Fig.  8,  and  along  the  chordse  tendinese,  which 
may  be  eroded  or  completely  ulcerated  through. 

Microscopically,  these  vegetations  are  seen  to  consist  of 
necrotic  tissue,  fibrin  deposited  from  the  blood  stream  in 
which  may  be  entangled  some  red  corpuscles  and  leucocytes, 
and  in  the  deeper  layers  leucocytes  and  proliferating  endo- 
thelial cells,  or  granulation  tissue.  Micro-organisms,  usually 
micrococci  in  large  masses,  are  invariably  present  in  the 
superficial  layers.  Vide,  Fig.  9.  The  necrotic  and  amorphous 
appearance  of  the  tissues  in  which  the  micro-organisms  are 
embedded  is  very  striking. 

In  certain  of  the  more  chronic  cases  the  vegetations 
may  assume  a  rounded,  opaque,  or  verrucose  form,  and  be 
of  considerable  size,  consisting  of  pale,  lobulated  excres- 
cences with  smooth,  rounded  surfaces.  Microscopically,  it 
will  be  seen  that  the  deeper  layers  consist  of  actively 
proliferating  endothelial  and  connective  tissue  cells  in 
process  of  organization  into  fibrous  tissue,  while  the  upper 
layers  consist  of  fibrin  and  leucocytes  more  or  less  necrotic 
and  amorphous,  with  few  nuclei,  staining  very  faintly. 
Micro-organisms  are  not  present  in  large  masses  on  the 
free  borders,  but  may  be  undiscoverable  or  very  difficult  to 
find,  and  only  revealed  after  careful  search  through  many 
sections.  If  found,  they  do  not  take  the  stain  well,  and 
appear  to  be  dead  or  moribund.  Because  of  this  absence 
or  scarcity  of  micro-organisms,  some  observers  have  held 
that  this  was  a  special  variety  of  simple  rheumatic 
endocarditis,  and  have  differentiated  it  under  the  name 
"  verrucose  endocarditis  "  (vide  Fig.  10).  These  "  verrucose  " 
vegetations   are,  however,  usually  found  in  cases   of  long 


"MALIGNANT"    OR   "PERNICIOUS"  ENDOCARDITIS.      71 

duration,  and  they  are  in  all  probability,  from  the  patho- 
logical appearances,  cases  in  which  the  disease  has  been 
wholly  or  partially  arrested  and  repair  is  taking  place,  but 
the  patient  succumbs  from  exhaustion  or  from  the  effect  of 
the  valvular  lesion. 

Besides  the  cardiac  lesions,  there  are  commonly  secondary 
lesions  in  the  spleen,  kidney,  or  brain,  due  to  embolism  from 
portions  of  the  vegetations  which  are  detached  from  the 
valves   and  lodge  in  the  smaller  arterioles.     In  the  organs 


FIG.   9.— SHOWING   MASSES   OF   MICRO-OEGANISMS   IN   THE   VALVES  (X   560). 

above  mentioned,  the  lodgment  of  an  embolus  in  one  of 
the  terminal  arterioles  causes  the  death  of  the  tissue  sup- 
plied by  that  branch,  as  there  is  insufficient  collateral 
circulation  to  nourish  the  part  when  its  blood  supply  is 
suddenly  cut  off.  The  portion  of  tissue  therefore  under- 
goes coagulation  necrosis,  and  the  resulting  condition  is 
known  as  an  "  infarct."  Infarcts  in  the  kidney  and  spleen 
are  usually  wedge-shaped,  but  may  be  of  irregular  outline, 


72 


HEART  DISEASE. 


FIG.    10. — MITRAL   VALVE,    SHOWING    "  VEBELCOSE  : 
VEGETATIONS. 


and    are    almost   invariably   ansemic,  i.e.  of  a   pale,   dead 
white  colour,  with  a  zone  of  congestion  round  the  nerotic 

area,  though  occa- 
sionally in  the 
spleen  they  are  red 
or  hsernorrhagic. 

Etiology. — Micro- 
organisms are  almost 
invariably  present  in 
abundance  in  the 
vegetations  on  the 
affected  valves,  where 
they  can  be  readily 
demonstrated  by  mi- 
croscopic examina- 
tion, and  they  can  frequently  be  isolated  in  pure  culture 
from  the  blood  of  the  patient  during  life.  They  are  usually 
micrococci.  Some  difference  of  opinion  exists  as  to  their 
nature,  and  as  to  whether  any  one  specific  micro-organism 
is  the  etiological  factor  in  this  disease.  Previous  to  the 
isolation  and  identification  of  the  diplococcus  isolated  in 
rheumatism,  various  observers  had  experimented  with  pure 
cultures  obtained  from  the  valves  in  malignant  endocarditis. 
By  injection  of  these  into  the  jugular  veins  of  animals, 
some  experimenters  with,  and  some  without  previous  injury 
to  the  valves,  had  produced  valvulitis,  in  some  instances 
accompanied  by  metastatic  infarcts.  The  organism  found 
was  not  the  same  in  all  cases.  Among  the  organisms 
which  have  been  isolated  from  cases  of  malignant  endocar- 
ditis are,  the  staphylococcus  aureus  and  albus,  and  citreus, 
the  streptococcus  pyogenes,  the  pneumococcus,  and  the 
gonococcus,  and  the  influenza  bacillus. 

In  1903,*  Poynton  and  Paine  read  an  important  paper, 
in  which  they  show   that  malignant  endocarditis  may  be 
*  Med.  Chir.  Trans.,  Vol.  85. 


"MALIGNANT"    OR   "PERNICIOUS"   ENDOCARDITIS.      73 

set  up  by  a  diplococcus,  indistinguishable  from  that  which 
they  have  isolated  in  rheumatic  fever.  They  give  an 
account  of  a  series  of  cases  of  pernicious  endocarditis, 
with  a  clinical  history  and  an  account  of  the  post-mortem 
examination,  in  which  they  obtained  from  the  affected 
valves  a  diplococcus,  cultures  of  which,  inoculated  into 
rabbits,  reproduced  pernicious  endocarditis  in  those 
animals.  This  diplococcus  they  considered  to  be  identical 
with  that  which  they  have  previously  isolated  in  cases  of 
pericarditis  and  endocarditis  associated  with  rheumatic 
fever.  By  inoculating  rabbits  with  an  attenuated  culture 
of  this  diplococcus  obtained  from  a  case  of  pernicious  en- 
docarditis, they  showed  that  it  might  give  rise  to  pericar- 
ditis without  valvulitis,  or  to  a  disease  indistinguishable 
from  rheumatic  fever.  Conversely,  by  inoculating  a  rabbit 
with  a  culture  of  a  diplococcus  originally  obtained  from  a 
case  of  rheumatic  fever,  the  virulence  of  which  had  been 
raised  by  passage  through  several  rabbits,  they  produced 
in  the  animal  well-marked  pernicious  endocarditis. 

In  all  the  cases  they  describe  in  this  paper  there  was 
a  history  of  rheumatic  fever  at  some  period  previous  to  the 
attack  of  pernicious  endocarditis. 

In  view  of  these  results,  it  is  only  fair  to  admit  that 
pernicious  endocarditis  may  in  some  cases,  if  not  in  a  large 
proportion,  be  due  to  infection  by  the  rheumatic  diplococcus, 
and  that  it  occurs  either  because  the  virulence  of  the  micro- 
organism is  great,  or  more  probably  because  the  resistance 
of  the  individual  attacked  is  very  low.  Injury  to  the  valve 
is  probably  an  important  etiological  factor,  for  in  the 
majority  of  cases  pernicious  endocarditis  affects  valves  which 
have  been  damaged  in  a  previous  attack  of  rheumatism. 

We  must  now  consider  the  role  played  by  other  micro- 
organisms which  have  been  met  with  in  this  disease. 

1.  The  Pyogenic  Organisms. — Numerous  observers  have 
testified  to  the  presence  of  the  streptococcus  pyogenes,  the 


74  HEART  DISEASE. 

staphylococcus  aureus  and  albus  in  the  vegetatioDS  on  the 
affected  valve  and  in  the  blood,  and  cultures  have  been 
made  from  the  blood  during  life  and  from  the  vegetations 
after  death. 

Of  these,  the  streptococcus  pyogenes  is  the  most  com- 
monly found,  and  next  in  frequency  the  staphylococcus 
aureus.  Combinations  of  two  of  these  organisms  are  also  fre- 
quently met  with,  e.g.  of  the  streptococcus  and  staphylococcus 
aureus,  or  albus,  or  of  the  staphylococcus  aureus  and  albus. 
If  we  admit  the  possibility  of  a  specific  rheumatic  diplococcus 
being  a  cause  of  pernicious  endocarditis,  it  is  probable  that 
it  may  frequently  be  one  of  the  organisms  in  a  mixed  infec- 
tion, but  not  be  recognized,  because  it  is  a  delicate  organism 
and  requires  special  culture  media  for  its  growth. 

It  is  a  remarkable  fact  that  while  many  observers 
have  succeeded  in  producing  endocarditis  in  rabbits  by 
inoculation  of  pure  cultures  obtained  from  a  case  of  pernicious 
endocarditis  in  man,  few  have  succeeded  in  producing  this 
condition  by  inoculation  of  cultures  of  the  streptococcus  or 
staphylococcus  pyogenes  obtained  from  other  sources,  e.g. 
cases  of  pyaemia  or  septicaemia.  Cole  *  has  succeeded  in 
doing  so  with  cultures  derived  from  puerperal  fever  and 
peritonitis,  as  already  mentioned.  Poynton  and  Paine  f 
made  several  attempts  with  different  brands  of  pyogenic 
organisms,  and  succeeded  in  some  instances,  but  the  usual 
result  was  septicaemia  and  the  early  death  of  the  inoculated 
animal.  Again,  though  ulcerative  endocarditis  is  met  with 
sometimes  in  cases  of  septicaemia,  pyaemia,  puerperal  fever, 
erysipelas,  osteomyelitis,  etc.,  it  is  the  exception  rather  than 
the  rule,  and  we  would  expect  it  to  be  very  common  were 
the  pyogenic  organisms  mainly  responsible  for  the  disease 
known  as  malignant  or  pernicious  endocarditis.  It  is  also 
remarkable  that  infarcts  in  this  affection  so  rarely  suppurate. 

*  Journ.  Infect.  Diseases,  vol.  i.  No.  4,  1004. 
t  Trans,  Med.  Chir.  Soc,  Vol.  85. 


"MALIGNANT"    OR   "PERNICIOUS"    ENDOCARDITIS.       75 

These  considerations  tend  to  support  the  view  of  Paine 
and  Poynton  that  pernicious  endocarditis  may  in  some 
instances  be  a  form  of  pernicious  rheumatism. 

The  Pneumococcus. — Pernicious  endocarditis  is  sometimes 
met  with  in  association  with  pneumonia  and  pneumococcal 
meningitis,  and  the  pneumococcus  has  been  frequently  iso- 
lated from  the  affected  valves.  Netter  *  has  written  several 
important  papers  on  this  subject,  and  has  produced  an 
ulcerative  endocarditis  in  rabbits  after  injury  to  a  valve 
by  inoculation  of  cultures  of  the  pneumococcus.  Michaelis  f 
has  also  produced  the  affection  in  dogs  by  repeated  inocula- 
tion of  cultures  of  the  pneumococcus  at  frequent  intervals. 
Osier,  Weichselbaum,  Huchard,  and  many  others  have 
published  cases  of  pneumococcal  endocarditis. 

We  must  therefore  admit  the  pneumococcus  as  one  of  the 
causes  of  pernicious  endocarditis,  though,  when  it  is  found, 
pneumonia  or  meningitis  is  usually  the  primary  disease. 

The  Gonococcus. — That  ulcerative  endocarditis  can  be 
caused  by  the  genococcus  was  first  shown  by  Gluzinski. 
Schedler,  His,  %  Councilman,^  and  others  have  confirmed 
his  observations.  Harris  ||  and  Johnson  have  recently 
described  two  cases  of  gonococcal  endocarditis,  and  in  a 
paper  read  before  the  Pathological  Society  in  April,  1905, 
Horder  describes  a  case  of  malignant  endocarditis,  in  which 
he  isolated  the  gonococeus  from  the  blood  during  life  and 
from  the  affected  valve  post  mortem. 

Pfeiffer's  Influenza  Bacillus. — Some  cases  of  ulcerative  en- 
docarditis due  to  this  organism  have  recently  been  described. 

Austin  1  has  published  an  account  of  three  cases  in 
which  he  found  Pfeiffer's  influenza  bacillus  in  the  affected 
valves.  Horder**  has  also  published  two  cases  which  he 
attributes  to  this  bacillus. 

*  Soc.  Anat.,  March,  1886 ;  Arch,  de  Phys.,  1886,  etc. 

t  Med.  Soc.  of  Berlin,  1895.  t  Berlin  Klin.  Woch.,  1892. 

§  Amer.  Jour.  Med.  Sc.,  1893.  ||  Joum.  Amer.  Phys.,  1902. 

^  John  Hopkins'  Reports,  1899.  **  Trans.  Path.  Soc,  April,  1905. 


76  BE  ART  DISEASE. 

Other  micro-organisms  which  have  occasionally  been 
found  in  the  affected  valves  in  pernicious  endocarditis 
are  the  bacillus  endocarditis  griseus  of  Weichselbaum,  the 
bacillus  capsulatus  of  the  same  author,  and  the  bacillus  coli. 

Pernicious  endocarditis  may  occur  as  a  complication  in 
scarlet  fever  and  smallpox,  and  in  erysipelas,  puerperal 
fever, 'pyaemia,  septicaemia,  esteomyelitis,  and  pneumonia,  as 
has  already  been  stated. 

Modes  of  Infection. — The  ways  in  which  the  micro- 
organisms which  attack  the  valves  may  obtain  admittance 
to  the  circulation  are  manifold :  by  the  skin,  as  in  cases  of 
open  wounds;  by  the  mucous  membranes  of  the  pharynx, 
especially  the  tonsils,  or  of  the  intestines ;  by  the  genito- 
urinary, and  by  the  respiratory  tracts.  All,  therefore,  may 
be,  at  one  time  or  other,  exposed  to  the  attacks  of  the 
pyogenic  microbes,  which  give  rise  to  this  form  of  endo- 
carditis, but  in  only  a  small  proportion  of  cases  are  the 
endocardial  tissues  specially  susceptible. 

Symptoms  and  Physical  Signs. — While  it  is  difficult  to  draw 
a  hard-and-fast  line  between  simple  and  pernicious  endocar- 
ditis, there  are  certain  clinical  features  which  may  be  said  to 
distinguish  the  latter.  These  are  prolonged  irregular  pyrexia 
of  a  septicemic  type,  the  occurrence  of  embolism,  change  in 
the  character  of  the  cardiac  murmurs,  progressive  anaemia 
aud  loss  of  flesh.     Rigors  may  occur,  but  are  not  common. 

The  age  of  the  patient  is  also  of  importance.  Malignant 
endocarditis  appears  to  be  a  disease  of  young  adult,  or 
middle  life,  and  is  rare  in  young  children.  From  an 
analysis  of  seventeen  cases  on  which  I  made  post-mortem 
examinations  during  the  years  1900  to  1904  at  St.  Mary's 
Hospital,  I  find  the  average  age  works  out  at  84.  Curiously 
enough,  this  almost  exactly  coincides  with  the  average  age 
arrived  at  by  Dreschfield  from  an  analysis  of  cases  during  a 
period  of  four  years  at  the  Manchester  Infirmary,  namely  34^. 

The  youngest  of  the  patients  in  the  St.  Mary's  cases  was 


"MALIGNANT"    OR   "PERNICIOUS"  ENDOCARDITIS.      77 

16,  the  oldest  54,  and  no  less  than  thirteen  out  of  seventeen 
were  between  the  ages  of  22  and  45. 

The  Temperature. — This  may  vary  considerably.  Some- 
times the  onset  is  insidious  and  the  temperature  is  little 
raised  above  normal,  ranging  from  99  to  100,  with  intervals  of 
apyrexia  for  some  clays.  Later  on,  as  the  symptoms  become 
more  pronounced,  the  temperature  ranges  high,  and  assumes 
a  septicemic  type,  running  up  to  102,  103,  or  104  in  some 
period  of  the  twenty-four  hours,  and  dropping  to  99  or  100  at 
another.  In  the  final  stages,  when  the  patient  is  exhausted 
by  the  disease,  it  is  frequently  subnormal  in  the  morning  and 


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TEMPERATURE    CHART  PROM    CASE   OP  PERNICIOUS   ENDOCARDITIS 

only  slightly  above  normal  in  the  evening.  Exacerbations 
of  temperature  usually  mark  the  occurrence  of  infarcts. 

The  above  temperature  chart,  from  the  later  stages  of 
a  severe  case,  shows  the  extreme  irregularity  of  tempera- 
ture that  may  occur. 

There  was  evidence  of  infarction  of  the  kidney  and  spleen 
respectively  when  the  temperature  rose  to  103°  and  104°  F. 
at  the  points  marked  A  and  B  on  the  chart. 

Infarction. — Infarction  of  the  spleen  will  commonly  be 
attended  with  pain  in  the  left  hypochondriac  region,  with 
tenderness  of  and  possibly  some  enlargement  of  the  spleen. 
Infarct  of  the  kidney  is  usually  marked  by  pain  in  the 
loin,  followed  by  hematuria  and  albuminuria,  but  these  may 


78  HEART  DISEASE. 

sometimes  be  absent,  and  hseroaturia  may  occur  as  a  result 
of  nephritis  without  infarction. 

Of  the  cerebral  vessels,  the  middle  cerebral  artery  is  the 
most  common  seat  of  embolism,  an  embolus  being  especially 
liable  to  lodge  where  it  divides  into  its  four  main  branches 
opposite  the  island  of  Eeil. 

Hemiplegia  may  result  with  aphasia  if  on  the  left  side  ; 
sometimes  this  may  pass  off  in  four  to  six  days  from  shrink- 
age of  the  embolus  or  establishment  of  some  collateral 
circulation.  In  a  case  of  which  the  specimen  is  in  the 
St.  Mary's  Hospital  Museum,  a  man  of  23,  suffering  from 
malignant  endocarditis,  suddenly  became  aphasic  and  lost 
all  power  in  his  right  side.  In  five  days  he  had  completely 
recovered  his  speech  and  almost  entirely  the  power  in  his 
limbs.  Post  mortem  the  embolus  was  found  to  have  lodged 
in  the  left  middle  cerebral  artery  where  it  divides  into  its 
main  branches.  The  embolus  had  apparently  shrunk,  and 
did  not  occlude  two  of  the  branches. 

Embolism  of  the  superior  mesenteric  artery  may  occur, 
o-iving  rise  to  gangrene  of  the  small  intestine,  with  symptoms 
of  collapse  and  shock  followed  by  profuse  melsena. 

Embolism  of  the  arteries  of  the  extremities  may  cause 
pain  and  temporary  numbness  with  pallor  and  coldness  of 
the  limb  if  a  large  vessel  is  blocked,  but  usually  collateral 
circulation  is  established  and  the  symptoms  pass  off. 

Aneurysms  are  occasionally  met  with  as  a  result  of 
lodgment  of  emboli  containing  micro-organisms  in  an  artery 
and  the  destructive  action  of  the  toxins  of  the  organisms  in 
the  vessel  wall.  They  may  be  multiple  or  single.  In  the 
St.  Mary's  Hospital  Museum  is  a  specimen  with  thirteen 
aneurysms  of  the  coronary  artery  of  the  heart.  I  have  seen 
two  instances  of  aneurysm  of  the  gluteal  artery,  and  one 
of  the  femoral,  and  aneurysms  of  the  cerebral  and  various 
other  arteries  have  been  described,  so  that  it  would  appear 
that  almost  any  artery  may  be  affected. 


"MALIGNANT"    OR   "PERNICIOUS"   ENDOCARDITIS.      79 

Infarcts  in  the  lung  are  exceptional,  not  merely  because 
the  disease  is  commonly  confined  to  the  left  side  of  the 
heart,  but  because  lodgment  of  an  embolus  in  a  small 
branch  of  the  pulmonary  artery,  if  the  valves  of  the  right 
side  of  the  heart  are  affected,  would  probably  not  cause  an 
infarct,  unless  there  is  in  addition  extreme  pulmonary  con- 
gestion from  back  working. 

Sometimes  numerous  capillary  embolisms  occur,  giving 
rise  to  petechia?  on  the  skin. 

The  Cardiac  Murmurs. — The  development  of  a  murmur 
in  association  with  a  previously  healthy  valve  will,  of  course, 
give  a  clue  to  the  condition,  but  not  infrequently  the  valve 
attacked  is  already  the  seat  of  a  previous  lesion,  and  a 
murmur  may  already  be  present.  Change  in  the  character 
of  the  murmur  should  be  carefully  watched  for  and  noted ; 
it  may  become  softer  and  weaker,  or  louder  and  musical. 
The  development  of  a  fresh  murmur  at  another  orifice  should 
also  be  looked  out  for. 

Anaemia  is  usually  pronounced  and  progressive,  and  the 
complexion  assumes  a  waxy  and  sallow  hue. 

The  Appetite  may  remain  good  and  the  tongue  clean  till 
a  very  late  stage  in  the  disease,  and  gastro-intestinal 
troubles  are  not  usually  marked,  though  diarrhoea  is  often 
present  in  the  septicemic  types. 

Diagnosis. — When  a  cardiac  murmur  of  recent  develop- 
ment is  present,  associated  with  pyrexia,  a  high  range  of 
temperature  of  an  irregular  or  septicemic  type  and  the 
occurrence  of  embolism  will  usually  enable  a  diagnosis  to  be 
made  early  in  the  course  of  the  disease.  The  persistence  of 
the  irregular  pyrexia,  the  progressive  anaemia,  the  sallow 
complexion,  loss  of  flesh,  and  occurrence  of  embolism,  will 
afford  confirmatory  evidence  of  the  malignant  character  of 
the  endocarditis.  In  young  children  we  frequently  meet 
with  prolonged  subacute  attacks  of  cardiac  rheumatism, 
in  which  a  valvular  murmur  may  be  present,  associated  with 


8o  HEART  DISEASE. 

pyrexia,  lasting  many  weeks  ;  but  in  these  cases  recurrent 
attacks  of  pericarditis  are  the  rule,  and  this,  with  the 
accompanying  myocarditis  leading  to  cardiac  dilatation,  is 
the  more  serious  malady,  and  is  readily  recognized.  It 
would,  indeed,  seem  that  in  young  children  we  have  a  type 
of  pernicious  pericarditis  corresponding  to  the  pernicious 
endocarditis  of  adults. 

When  no  murmur  exists,  or  when  a  valvular  murmur  of 
old  standing  is  present,  in  association  with  pyrexia  of  unex- 
plained cause,  a  differential  diagnosis  may  have  to  be  made 
from  typhoid  fever,  septicaemia,  and  acute  miliary  tubercu- 
losis. Typhoid  can,  after  a  week  or  ten  days,  be  identified 
by  the  eruption  of  spots,  abdominal  symptoms,  condition  of 
the  tongue,  and  Widal's  reaction.  Septicaemia,  in  the 
ordinary  sense  of  the  term,  may  be  usually  traced  to  some 
source  of  septic  infection,  but  inasmuch  as  pernicious  endo- 
carditis is  a  septicaemia  complicated  by  a  valvular  lesion, 
it  is  out  of  place  to  use  the  term  "  differential  diagnosis  "  in 
this  connection.  In  acute  miliary  tuberculosis,  if  we  cannot 
discover  any  old  tubercular  lesion,  we  may  have  to  wait  till 
definite  signs  in  the  lungs  or  the  onset  of  tubercular 
meningitis  disclose  its  nature. 

Change  in  the  character  of  a  pre-existing  murmur,  or 
the  development  of  a  valvular  murmur,  and  the  occurrence 
of  embolism  will  usually,  sooner  or  later,  make  clear  the 
nature  of  the  malady  in  pernicious  endocarditis. 

In  the  acute  cases  cultures  of  micrococii  can  frequently 
be  made  from  10  c.c.  of  blood  withdrawn  under  aseptic 
precautions  by  a  sterile  syringe  from  the  median  basilic  vein, 
and  inoculated  into  suitable  culture  media. 

It  must  be  borne  in  mind  that  possibly  the  rheumatic 
diplococcus  is  responsible  for  a  certain  number  of  cases,  and 
the  culture  media  must  be  selected  accordingly.  These 
micro-organisms  do  not  flourish  in  broth  or  on  agar,  though 
they   may   grow   feebly,    but,   according   to   Poynton   and 


"MALIGNANT"    OR    "PERNICIOUS"  ENDOCARDITIS.      Si 

Paine,  grow  best  in  milk,  so  this,  or  blood  agar,  on  which 
Shaw  *  finds  they  grow  freely,  should  be  included. 

Prognosis. — The  prognosis  is,  as  the  name  implies,  very 
grave.  In  the  acute  cases,  when  the  temperature  ranges 
high,  and  embolism  takes  place  early,  recovery  is  rare,  and 
the  disease  may  prove  fatal  in  a  few  weeks.  In  the  more 
chronic  cases  of  insidious  onset,  unexpected  recovery  some- 
times takes  place  after  the  lapse  of  two  months  or  more, 
when  the  patient  seems  almost  reduced  to  the  last  extremity. 
That  a  certain  proportion  of  cases  recover  in  which  severe 
ulceration  of  the  valves  has  taken  place,  attended  with 
infarction  of  the  kidney  or  spleen,  is  demonstrated  from 
time  to  time  by  post-mortem  examinations,  in  which  greatly 
deformed  cicatrized  valves  or  cicatrices  on  the  endocardium 
and  old  cicatrized  infarcts  are  found  some  years  later.  In 
a  large  group  of  cases,  in  which  there  is  no  evidence  of 
infarction,  the  lesions  found  in  the  valves  indicate  that 
extensive  ulceration  and  destruction  must  have  taken  place 
during  the  attack  of  acute  endocarditis.  The  two  last- 
mentioned  groups  could  scarcely  be  classified  as  "malig- 
nant," inasmuch  as  the  acute  disease  did  not  prove  fatal, 
though  they  were  undoubtedly  instances  of  "  ulcerative 
endocarditis."  The  question  of  prognosis  will  therefore  vary 
with  the  degree  of  virulence  of  the  causative  micro-organ- 
ism and  the  resistance  of  the  individual,  as  evidenced  by  the 
formation  of  protective  substances  in  the  blood,  or  the  reverse. 

Treatment. — Various  drugs  have  been  tried  without  any 
appreciable  result.  Salicylates  are  useless  :  salol,  sulpho- 
carbolate  of  soda,  and  benzoate  of  soda  have  been  freely 
given,  but  have  not  proved  to  be  of  service.  Perchloride  of 
mercury,  administered  freely,  has  seemed  to  be  efficacious 
in  some  cases.  General  tonics,  such  as  iron  quinine  and 
strychnine,  are  of  most  value,  as  they  help  to  maintain  the 

*  Etiology    of    Acute    Rheumatic   Fever,   Journal  of    Path,  and  Bad. 
December,  1903. 


82  HEART  DISEASE. 

strength,  of  the  patient,  though  they  are  not  in  any  sense 
a  specific  remedy.  Citric  acid  may  be  given  with  advantage, 
as  it  reduces  the  coagulability  of  the  blood  by  combining 
with  the  calcium  salts,  and  thereby  lessens  the  tendency  to 
formation  of  clot  on  the  diseased  valve  and  the  chances 
of  embolism.  Possibly  thymus  gland  may  be  of  service  by 
stimulating  the  production  of  leucocytes. 

Good  results  have  been  claimed  from  time  to  time  by 
various  authors  from  the  injection  of  antistreptococcic 
serum.  As  the  disease  may  be  set  up  possibly  by  the 
rheumatic  organism,  possibly  by  streptococci,  or  pneumo- 
cocci,  or  gonococci,  it  is  obvious  that  the  indiscriminate 
use  of  a  so-called  antistreptococcic  serum  is  not  rational 
or  scientific,  even  if  one  were  sure  that  the  serum  really 
possessed  any  antitoxic  substances,  and  this  we  have  as 
yet  no  accurate  means  of  determining. 

CHBONIC  ENDOCARDITIS. 

Under  this  heading  are  comprised  certain  chronic  de- 
generative changes  in  the  valves  which  set  in  insidiously 
in  later  life,  and  are  usually  associated  with  degenerative 
changes  in  the  aorta.  They  are  to  be  distinguished  from 
chronic  valvular  lesions,  which  are  the  result  of  cicatrization 
after  an  attack  of  acute  endocarditis. 

Morbid  Anatomy. 
The  valves  become  thickened  and  opaque  and  lose  their 
elasticity.  The  aorta  is  usually  dilated  and  atheromatous. 
The  aortic  valves  are  chiefly  affected,  and  though  there  is 
no  actual  loss  of  substance,  the  rigidity  of  the  cusps,  together 
with  the  dilatation  of  the  aorta,  occasions  a  certain  degree  of 
incompetence.  Sometimes  calcareous  plates  may  be  present 
in  the  aorta  at  the  root  of  the  valves,  and  project  into  the 
cusps  themselves.  A  certain  degree  of  obstruction  may  result, 
giving  rise  to  a  systolic  aortic  murmur,  but  this  may  be  due  to 


CHRONIC  ENDOCARDITIS.  S3 

roughening-  of  the  valves  without  actual  stenosis.  The  mitral 
valve  is  affected  to  a  less  degree  than  the  aortic,  but  becomes 
thickened  and  opaque,  and  slight  incompetence  may  result. 

Etiology. — Among  the  recognized  causes  of  chronic 
degenerative  valvular  lesions  are  lead  poisoning,  gout, 
kidney  disease,  and  what  Murchison  termed  lithfemia,  from 
excessive  eating  and  drinking  with  defective  elimination. 
These  are  conditions  associated  with  high  arterial  tension, 
involving  constant  undue  strain  on  the  aorta  and  its  valves. 

Valvular  change  of  like  character  is  common  in  men 
following  certain  arduous  occupations,  such  as  those  of  the 
miner,  collier,  blacksmith,  hammerman,  and  soldier.  Here  we 
have  undue  intermittent  pressure  within  the  aorta.  As  was 
pointed  out  by  Clifford  Allbutt,  Fothergill,  and  others,  in  the 
occupations  mentioned  the  undue  pressure  is  created  by  effort 
in  a  constrained  and  cramped  position,  or  by  work  of  such 
a  character  as  to  require  prolonged  closure  of  the  glottis 
and  fixation  of  the  chest  by  holding  the  breath,  or  by  violent 
muscular  exertion  constantly  repeated  throughout  the  day. 

Heredity  is  an  important  factor  in  connection  with  high 
arterial  tension,  due  to  gout  or  lithseinia,  as  the  tendency 
may  be  transmitted  through  many  generations. 

Age. — Degenerative  changes  in  the  valves  usually  set  in 
after  middle  life,  from  the  age  of  40  to  45  onwards,  and  are 
frequently  associated  with  degenerative  changes  in  the 
aorta  or  cerebral  vessels. 

In  later  life,  apart  from  actual  disease,  there  is  a  ten- 
dency to  thickening,  opacity,  and  loss  of  elasticity  in  the 
valves,  which  in  some  instances  may  give  rise  to  a  murmur. 

Syphilis  may  be  incriminated  in  a  certain  proportion  of 
cases,  especially  where  degenerative  changes  occur  early  in 
life. 

The  symptoms  and  physical  signs  vary  according  to  the 
valve  affected,  and  are  discussed  later  in  the  chapters  on 
the  different  valvular  lesions. 


CHAPTER  VI. 

ETIOLOGY    OF   VALVDLAIi    LESIONS. 

Acute  Endocarditis. — This  is  by  far  the  most  common  cause 
of  valvular  lesions.  This  has  already  been  fully  discussed 
in  a  previous  chapter.  The  acute  inflammatory  process 
may  rapidly  impair  the  efficiency  of  the  valve  and  render 
it  incompetent.  Subsequent  cicatricial  contraction  of  the 
fibrous  tissue  formed  in  the  process  of  repair  may  still 
farther  impair  its  efficiency,  or  give  rise  to  progressive 
stenosis,  which  may  result,  in  extreme  cases,  in  a  narrow 
funnel-shaped  rigid  orifice  less  than  half  an  inch  in  diameter. 

Chronic  Endocarditis, — Chronic  endocarditis  is  an  in- 
sidious affection  occurring  in  middle  or  later  life,  usually 
due  to  high  arterial  tension,  whether  from  gout,  kidney 
disease,  or  other  causes,  and  intimately  associated  with 
the  degenerative  change  known  as  atheroma  of  the  aorta. 
The  valves  become  thickened,  and  lose  their  elasticity,  and 
incompetence  usually  results  from  this  in  conjunction  with 
dilatation  of  the  aorta.  Syphilis  may  be  a  cause,  especially 
when  atheroma  of  the  aorta  occurs  early  in  life,  associated 
with  degenerative  change  in  the  valves. 

Rupture  of  a  Valve. — Rupture  of  a  valve  is  of  rare 
occurrence.  It  is  usually  the  aortic  valve  which  suffers, 
and,  except  as  a  result  of  direct  violence,  the  rupture  will 
nearly  always  have  been  preceded  by  disease  in  its 
structure,  and  by  the  cause  of  such  disease,  high  arterial 
tension.  The  rupture  usually  takes  place  during  some 
severe  muscular   exertion,  and  is  attended  by  great  pain 


ETIOLOGY  OF   VALVULAR  LESIONS.  85 

in  the  region  of  the  heart.  It  may  be  a  complete  or  partial 
rupture  of  one  of  the  cusps  of  the  aortic  valve,  or  may  be  a 
mere  slit  in  it. 

One  or  more  tendinous  cords  of  the  mitral  valve  may  be 
found  ruptured  when  this  valve  has  been  the  seat  of  disease  ; 
but  this  occurrence  can  rarely  be  dated  by  any  recognized 
accession  of  symptoms,  though  it  must  give  rise  to  a  con- 
siderable increase  in  the  derangement  of  the  circulation. 

Dilatation  of  the  Orifice  of  a  Valve. — Dilatation  of  the 
orifice  may  upset  the  functional  efficiency  of  a  valve  while 
the  valve  itself  has  not  undergone  any  material  change. 
The  aortic  orifice  is  less  liable  to  be  stretched  and  enlarged 
than  the  mitral,  as  would  be  expected  from  the  difference 
in  the  structures  surrounding  the  two.  It  is  only  com- 
paratively late  in  life  that  the  strong  fibrous  ring  at  the 
root  of  the  aorta  ever  yields,  and  it  will  then  only  take 
place  as  part  of  a  general  dilatation  of  the  first  part  of 
this  vessel,  the  result  of  atheroma  or  chronic  degenerative 
changes.  The  usual  result  is  more  or  less  insufficiency 
or  regurgitation;  but,  paradoxical  as  it  may  appear,  there 
may  actually  be  obstruction  as  well,  the  valves  being  rigid 
and  projecting,  even  during  systole,  across  the  dilated 
mouth  of  the  aorta. 

Mitral  insufficiency  from  failure  of  fairly  healthy  valves 
to  close  the  orifice  is  not  uncommon.  Sometimes  the 
orifice  is  very  much  enlarged,  admitting  four  or  five  fingers 
instead  of  three.  Frequently,  however,  there  is  no  stretch- 
ing of  the  opening,  and  the  valves  themselves  are  un- 
affected, although  during  life  there  has  certainly  been 
regurgitation.  Various  explanations  of  this  fact  have  been 
offered.  It  has  been  supposed  that  irregular  action  of  the 
papillary  muscles  interferes  with  the  accurate  adjustment 
of  the  valvular  curtains ;  and,  again,  that  the  papillary 
muscles,  being  carried  by  dilatation  of  the  ventricle  so  far 
from  the  valvular  ring  that  the  tendinous  cords  are  dragged 


86  HEART  DISEASE. 

down  too  far,  do  not  allow  the  margins  of  the  valves  to  meet 
during  the  systole. 

The  real  cause  of  the  imperfect  closure  of  the  valves 
is  that  originally  suggested  by  Donald  McAlister.*  He 
pointed  out  that  an  important  factor  in  the  valvular 
mechanism  is  the  active  contraction  of  the  mitral  orifice 
with  the  systole  of  the  ventricle.  We  are  accustomed  to 
imagine  that  this  opening,  like  the  aortic,  is  surrounded  by 
a  strong  fibrous  ring,  maintaining  its  form  and  patency 
under  all  circumstances  ;  but  this  is  not  the  case,  as  was 
shown  by  Sibson  in  dissections  and  specimens,  which  I  had 
the  pleasure  of  assisting  him  to  prepare ;  for  it  was  demon- 
strated that  the  mitral  ring  of  fibrous  tissue,  taking  its 
origin  from  the  central  fibro-cartilage  of  the  heart,  gradually 
thins  out  till  at  the  opposite  side  of  the  orifice  it  is  practically 
non-existent.  There  is  nothing,  therefore,  to  keejD  the  mitral 
orifice  rigid,  or  prevent  it  from  altering  its  shape  ;  hence  we 
find  that,  during  systole,  the  transversely  circular  fibres  of 
the  cardiac  muscle,  by  their  contraction,  cause  a  narrowing 
of  the  mitral  orifice,  and  partially  close  it  independently  of 
the  valves.  Such  a  closure  is  in  effect  a  part  of  the 
general  obliteration  of  the  ventricular  cavity  during  systole. 
When,  therefore,  there  is  dilatation  of  the  ventricle,  this 
active  constriction  of  the  auriculo-ventricular  opening  is 
imperfectly  performed,  and  the  valve  fails  to  cover  the 
whole  area  of  the  orifice. 

Mitral  regurgitation  caused  in  this  way,  may  occur  at 
any  period  of  life,  and  under  very  different  conditions.  The 
cardiac  dilatation  may  be  the  result  of  imperfect  nutrition 
in  advancing  years,  or  of  debilitating  influences,  or  it  may 
be  induced  by  acute  disease,  such  as  enteric  fever  or  acute 
rheumatism.  Perhaps  the  most  common  and  important 
cause  is  aneeinia ;  it  is  most  important  because  of  its  fre- 
quency in  young  adults,  and  because,  though  curable,  it 

*  British  Medical  Journal,  August,  18S2. 


ETIOLOGY  OF   VALVULAR  LESIONS.  87 

is  yet  liable  to  be  rendered  permanent  by  imprudence 
and  neglect.  George  Balfour  has  rendered  good  service  by 
calling  attention  to  this  condition  under  the  head  of 
"  Curable  Mitral  Regurgitation."  Now,  although  weakness 
of  the  cardiac  muscular  fibres,  or  want  of  energy  in  their 
contraction,  is  perhaps  an  essential  condition  in  the  pro- 
duction of  dilatation,  another  factor  plays  an  important 
part,  namely,  high  arterial  tension.  We  should  not  expect 
anaemia  to  be  attended  with  any  such  state  of  the  circulation, 
but  this  is  very  frequently  the  case  in  the  ordinary  type. 

Pernicious  anaemia,  however,  is  less  commonly  attended 
with  high  arterial  tension,  perhaps  because  of  the  frequent 
intercurrent  attacks  of  pyrexia ;  for  pyrexia,  as  is  well 
known,  relaxes  arteries  and  lowers  the  arterial  tension. 

It  may  be  remarked  in  passing,  that  the  low  arterial 
tension  which  accompanies  pyrexia  probably  renders  the 
occurrence  of  dilatation  of  the  ventricle  much  less  frequent 
in  acute  disease  than  we  should  expect  as  a  result  of  the 
debilitating  effect  of  the  accompanying  myocarditis  or 
"  cloudy  swelling  "  of  the  muscular  walls  of  the  heart. 

Mitral  incompetence  may,  further,  be  a  secondary  con- 
sequence of  aortic  incompetence,  through  the  dilatation  of 
the  left  ventricle.  But,  unless  cardiac  debility  have  a  share 
in  the  production  of  this  dilatation,  a  comparison  between 
it  and  the  dilatation  just  spoken  of  is  illusory.  The  one  is 
the  result  of  asthenia,  the  other  of  over-distension  of  the 
ventricular  cavity ;  in  the  one,  the  contraction  of  the 
ventricle  is  never  completed ;  in  the  other,  it  is  carried 
through  energetically. 

Congenital  Valvular  Affections. — Lesions  of  one  or  more 
of  the  valves  of  the  heart  are  sometimes  found  at  birth. 
They  may  be  the  result  of  a  congenital  malformation,  or 
of  endocarditis  occurring  while  the  foetus  was  in  utero.  In 
the  former  case  the  pulmonic  valve  is  most  commonly  at 
fault,  the  lesion  being  usually  constriction    of  the  orifice, 


HEART  DISEASE. 


and  frequently  the  valvular  defect  is  associated  with  a 
malformation  of  some  other  portion  of  the  heart.  In  the 
latter  case  the  valves  of  the  right  side  of  the  heart  usually 
suffer,  but  those  of  the  left  side  may  also  be  affected,  the 
aortic  more  commonly  than  the  mitral. 


CHAPTER   VII. 
YALYULAE  LESIONS. 

POINTS  TO  BE  CONSIDEEED  IN  STUDYING  A  CASE  OF 
VALVULAE  DISEASE — THE  PHYSICAL  SIGNS— CAEDI  AC 
MUEMUES,  THEIE  SIGNIFICANCE  AS  EEGAEDS  THE  SEAT 
AND  AS  EEGAEDS  THE  EXTENT  OF  THE  LESION  — 
MODIFICATION  OF  HEAET-SOUNDS  —  THE  PULSE,  ITS 
IMPOETANCE    IN   DIAGNOSIS. 

Diseases  of  the  heart  are  classified  as  structural  and 
valvular,  according  as  the  morbid  change  affects  the 
muscular  walls  or  the  valves.  There  are,  again,  functional 
derangements  which  must  be  included  among  the  affec- 
tions of  the  heart. 

The  valvular  lesions  will  be  first  discussed:  they 
are  what  is  usually  understood  by  heart  disease,  and  are 
most  important  because  most  numerous.  We  know  more 
about  them,  and  can  be  more  certain  of  their  diagnosis, 
thanks  to  the  murmurs  to  which  alterations  in  the  valves 
give  rise.  We  are  also  in  a  better  position  to  estimate 
the  extent  of  the  lesion,  and  to  give  an  accurate  prognosis 
in  valvular  disease  than  in  structural.  The  estimation  of 
the  obstruction  produced  by  a  certain  degree  of  narrowing 
of  one  or  other  orifice,  or  of  the  amount  of  reflux  resulting 
from  incompetence  of  a  given  valve,  is  a  problem  of  hydro- 
statics capable  of  solution,  but  no  such  definite  conclusion 
can  be  arrived  at,  when  in  structural  disease  we  have  to 
form  an  opinion  as  to  the  contractile  power  and  durability 
of  muscular  fibres  in  a  certain  stage  of  degeneration. 


9o  HEART  DISEASE. 


The  Clinical  Study  of  Yalvulae  Disease. 

In  studying  a  case  of  valvular  disease  of  the  heart, 
the  following  are  the  points  which  must  be  taken  into 
consideration : — 

1.  The  valve  affected,  and  the  relative  danger  attaching 

to  the  particular  lesion. 

2.  The   actual  condition  of  the  orifice  and  valve — the 

degree  of  obstruction  or  amount  of  regurgitation  to 
which  the  lesion  has  given  rise. 

3.  The   origin    of   the    lesion,    whether    due    to    acute 

rheumatism,  degenerative  changes,  or  other  causes. 

4.  The  degree  of  soundness  and  vigour,  functional  and 

nutritional ;  firstly,  of  the  muscular  substance  of 
the  heart  itself;  secondly,  of  the  tissues  generally. 
How  far,  in  fact,  and  for  how  long  compensatory 
changes  can  be  counted  upon.  In  considering  this 
question,  family  history  will  have  an  important 
place. 

Localization  of  the  Valvular  Disease. — Significance 
of  the  Cardiac  Murmurs. 

The  chief  guide  in  localizing  disease  in  the  valves  of 
the  heart  is  a  murmur,  produced,  either  by  obstruction  to 
the  current  of  blood  when  one  or  other  orifice  is  narrowed 
or  roughened,  or  by  regurgitation  of  the  blood  when  a 
valve  no  longer  closes  perfectly.  The  term  stenosis  or 
constriction  is  employed  to  denote  the  condition  of  an 
orifice  which  is  narrowed,  the  result  of  the  narrowing  being 
obstruction :  the  term  insufficiency  or  incompetence  is 
employed  to  characterize  the  state  of  a  valve  which  fails  to 
close  the  opening  it  ought  to  protect,  while  regurgitation 
or  reflux  expresses  the  functional  effect.  It  is  well,  as  far 
as  possible,  to  observe  the  distinction  between  the  names 


THE   CARDIAC  MURMURS.  91 

indicative  of  structural  change  and  those  expressive  of 
functional  derangement  resulting  therefrom,  but  the  terms 
"  obstruction  "  and  "  regurgitation  "  are  in  such  familiar  use 
that  they  are  frequently  employed  when  "stenosis"  and 
"  insufficiency  "  would  be  more  exact. 

By  means  of  the  murmurs  we  learn  definitely  which 
valve  is  affected  and  what  is  the  nature  of  the  affection — 
whether  such  as  to  produce  obstruction  or  regurgitation — 
but  they  fail  altogether  by  themselves  to  indicate  the 
amount  of  damage  which  a  valve  has  sustained.  A  loud 
murmur  may  be  produced  by  a  very  slight  change,  and 
a  murmur  which  is  scarcely  audible  may  be  indicative  of 
extensive  destruction  of  valves.  Some  information,  however, 
may  be  gathered  from  a  careful  study  of  murmurs. 

Different  Characters  of  Murmurs  :  their  Value  as 
regards  Estimation  of  the  Extent  of  the 
Valvular  Lesion. 

Murmurs  may  be  compared  or  contrasted  in  several 
respects  :  in  intensity,  they  may  be  loud  or  soft ;  in  duration, 
they  may  be  long  or  short ;  they  may  be  blowing,  or  musical, 
or  mixed,  rough  and  vibratory,  or  smooth.  Again,  they  may 
begin  with  an  accent,  or  rise  gradually  to  a  maximum 
intensity. 

A  loud  murmur  is,  on  the  whole,  of  less  serious  import 
than  one  which  is  weak  and  soft.  It  is,  at  any  rate, 
indicative  of  force  in  the  heart's  action,  and  of  vigour  in  the 
movement  of  the  blood ;  and  weakness  of  the  heart  con- 
stitutes the  greatest  of  all  dangers.  Then,  again,  although 
a  rough  edge  to  a  large  opening  in  aortic  or  mitral 
incompetence  may  generate  vibrations  which  will  produce 
a  loud  murmur,  a  mere  slit  in  a  membranous  valve,  or  a 
shred  of  fibrin  hanging  by  one  end,  is  more  likely  to  have 
such  an  effect. 


92  HEART  DISEASE. 

In  a  case  seen  with.  Dr.  Parrott  of  Hayes,  a  systolic 
mitral  niurinur,  of  such  intensity  as  to  be  heard  distinctly 
across  a  billiard-table,  had  been  present  for  fifteen  or  twenty 
years  without  giving  rise  to  symptoms,  until  dilatation  of 
the  heart  was  induced  by  extreme  over-exertion.  Another 
very  loud  murmur  which  came  under  my  notice  was  attended 
with  no  important  symptoms  for  the  several  months  during 
which  the  patient  was  under  observation.  It  was  systolic 
aortic,  and  could  be  heard  half  a  yard  or  more  from  the 
chest,  through  the  man's  clothes.  In  another  case,  a 
murmur  almost  as  loud  was  found,  after  death,  to  be  due 
to  a  delicate  fibrinous  thread  at  the  free  margin  of  one  of 
the  aortic  valves. 

On  the  other  hand,  cases  are  met  with  in  which  the 
pulse  may  indicate  serious  aortic  regurgitation  while  no 
diastolic  murmur  can  be  heard,  and  a  murmur  gradually 
develops  itself  as  the  patient  gains  strength  and  recovers 
from  a  state  of  extreme  prostration;  and  it  is  common  in 
mitral  stenosis  for  murmurs  to  disappear  with  the  super- 
vention of  serious  symptoms,  and  to  reappear  as  these  are 
abated  by  treatment.  It  must  not  be  concluded  that  a  soft 
or  weak  murmur  is  necessarily  indicative  of  either  a  failing 
heart  or  greatly  damaged  valve ;  but  a  diminution  in  the 
intensity  of  a  murmur,  gradual  or  sudden,  may  confirm 
unfavourable  indications  given  by  symptoms. 

The  character  of  a  murmur — its  roughness  or  vibratory 
character  or  smoothness — may  have  diagnostic  significance, 
as  will  be  pointed  out  later,  but  it  does  not  give  any  infor- 
mation with  regard  to  the  extent  of  structural  change  or 
functional  derangement.  A  musical  murmur  would  seem 
to  require  for  its  production  either  a  very  fine  chink  with 
thin  margins,  or  a  thin  membrane  capable  of  vibrating  like 
a  string,  and  would  therefore  seem  to  be  inconsistent  with 
serious  disease  ;  but  this  cannot  be  laid  down  as  an  absolute 
rule.   A  musical  note  is  often  heard  in  the  midst  of  a  blowing 


MODIFICATIONS  OF  THE  SOUNDS   OF  THE   HEART.      93 

murmur  or  at  the  beginning  or  end  of  such  a  murmur.  A 
long  murmur,  except  in  the  case  of  mitral  or  aortic  stenosis, 
is  usually  indicative  of  early  and  comparatively  slight  dis- 
ease and  of  efficient  action  of  the  heart.  A  short  murmur 
may  be  innocent  of  prognostic  import,  but  it  is  very 
frequently  an  indication  of  ruined  valves  and  of  a  failing 
heart :  it  may,  for  instance,  indicate  that  the  orifice  is  so 
patent,  say,  in  aortic  insufficiency,  that  the  refluent  blood 
passes  through  it  rapidly  and  with  little  hindrance  ;  or  in 
mitral  disease,  that  the  systole  is  brief  and  imperfect,  the 
heart  being  on  the  point  of  breaking  down. 

The  accent  at  the  beginning  of  a  murmur  is  chiefly 
observed  in  the  regurgitant  diastolic  murmur  of  aortic 
insufficiency  where  it  represents  the  second  sound,  and  it 
is  important  as  showing  that  the  valves  still  act  as  a  check 
on  the  reflux  of  blood  from  the  aorta.  It  has  the  same 
significance  in  a  minor  degree  as  persistence  of  the  aortic 
second  sound — a  very  important  fact,  which  will  be  fully 
explained  later,  in  the  chapter  on  aortic  regurgitation. 

It  will  thus  be  seen  that  the  murmurs,  while  pointing 
out  distinctly  and  certainly  what  valve  is  affected,  afford  also 
some  information  as  to  the  extent  of  change  which  has 
taken  place,  though  only  of  a  vague  character. 

Modification  of  Heaet-Sounds. 

The  heart-sounds  may  be  modified  by  murmurs  in 
various  ways.  A  mitral  systolic  or  an  aortic  diastolic 
murmur  may  accompany,  replace,  or  follow  the  sound  with 
which  it  is  associated  in  the  cardiac  cycle.  Generally 
speaking,  when  the  heart-sound  is  distinctly  heard  as  well 
as  the  accompanying  murmur,  the  lesion  is  slight :  when, 
on  the  contrary,  it  is  entirely  replaced  by  the  murmur,  the 
lesion  is  probably  severe. 

When  a  mitral  murmur  follows  the  first  sound  at  a  brief 


94  HEART  DISEASE. 

but  appreciable  interval,  constituting  a  "  retarded  systolic  " 
murmur,  it  seems  to  show  that  the  valves  come  together 
accurately  at  first,  but  fail  to  remain  in  apposition  through- 
out the  whole  period  of  the  ventricular  contraction.  It 
indicates,  therefore,  that  the  changes  in  the  valves,  and 
consequently  the  amount  of  leakage,  can  only  be  slight. 
A  "  retarded  diastolic "  aortic  murmur  is  sometimes  met 
with,  but  it  has  not  the  same  favourable  significance. 

The  first  sound  in  association  with  the  presystolic 
murmur  of  mitral  stenosis  may  be  greatly  modified.  It  is 
not  replaced  by  the  murmur,  but  is  usually  altered  in 
character,  becoming  short,  sharp,  and  high-pitched. 

The  Pulmonic  Second  Sound. 

i 

This  is  usually  accentuated  to  a  varying  degree  in 
mitral  affections,  owing  to  increase  of  pressure  in  the 
pulmonary  circulation.  There  are  two  factors  instrumental 
in  causing  this  increase  of  pressure — obstruction  to  the 
outflow  of  blood  from  the  pulmonary  veins  into  the  left 
auricle,  due  to  the  mitral  lesion;  and  increased  driving 
power  of  the  right  ventricle,  the  result  of  compensatory 
hypertrophy.  The  degree  of  accentuation  of  the  pulmonic 
second  sound  depends  on  the  degree  of  pressure  in  the 
pulmonary  circulation :  it  will  thus  afford  important 
evidence  as  to  the  amount  of  reflux  or  obstruction  caused 
by  the  mitral  lesion,  and  also  as  to  the  state  of  efficiency 
of  the  right  ventricle.  For  instance,  if  in  a  case  of 
mitral  disease  the  pulmonic  second  sound  is  greatly 
accentuated,  it  will  tend  to  show  that  the  mitral  lesion  is 
one  of  some  severity,  and,  as  confirmatory  evidence,  we 
should  expect  to  find  hypertrophy  of  the  right  ventricle. 
Bronchitis,  or  any  intercurrent  lung  trouble,  increasing  the 
obstruction  to  the  flow  of  blood  through  the  lungs,  will 
tend  to  cause  still   greater  accentuation  of  the  pulmonic 


ALTERATIONS  IN   THE   CARDIAC  RHYTHM.  95 

second  sound,  provided  that  the  right  ventricle  does  not 
break  down  under  the  strain.  If  in  a  severe  case  of  mitral 
disease  the  pulmonic  second  sound,  from  being  greatly 
accentuated,  becomes  feeble  or  much  diminished  in  in- 
tensity, it  will  indicate,  not,  of  course,  that  the  valvular 
lesion  is  less,  but  that  the  right  ventricle  is  beginning  to 
fail. 

The  aortic  second  sound  will  be  accentuated  when  the 
tension  in  the  systemic  circulation  is  high  from  any  cause ; 
it  will  be  altered  in  intensity  and  pitch  in  aneurysm,  or  in 
dilatation  of  the  aorta. 

Reduplication  of  Heart-Sounds. 

Reduplication  of  the  second  sound  heard  at  the  apex  of 
the  heart  indicates  that  the  pulmonic  and  aortic  valves 
do  not  close  synchronously.  It  is  of  common  occurrence 
in  mitral  disease,  especially  in  mitral  stenosis,  when  it 
indicates  that  the  pressure  in  the  pulmonary  circulation 
has  become  so  considerable  as  to  cause  the  pulmonic  valves 
to  close  before  the  aortic. 

Reduplication  of  the  first  sound  heard  at  the  apex  in- 
dicates that  the  two  ventricles  do  not  accomplish  their 
systole  simultaneously,  owing  to  the  fact  that  one  is 
beginning  to  give  way  under  extra  strain  imposed  on  it. 
It  is  not  infrequently  met  with  in  advanced  aortic  stenosis, 
or  in  cases  of  high  arterial  tension,  such  as  results  from 
kidney  disease;  it  will  then  show  that  the  left  ventricle 
is  beginning  to  fail. 

Alterations  in  the  Cardiac  Rhythm. 

Intermission  is  less  frequent  than  irregularity  as  a  result 
of  valvular  disease.  The  particular  affections  in  which 
this  deviation  from  the  normal  rhythm  is  most  liable  to 
occur  are  aortic  incompetence,  when  it  indicates  a  faltering 


96  HEART  DISEASE. 

of  the  heart's  action,  and  certain  functional  disturbances 
due  to  a  reflex  from  gastric  troubles.  Irregularity  is 
very  common  as  a  result  of  mitral  incompetence,  when  it 
is  not  of  serious  import.  It  may  also  occur  in  association 
with  fibroid  degeneration  of  the  heart  walls  in  conjunction 
with  general  arterio-sclerosis,  when  the  prognosis  is  grave, 
as  death  may  occur  from  a  syncopal  attack,  or  hemiplegia 
result  from  rupture  of  a  cerebral  vessel. 


THE   PULSE. 

Information  to  be   gathered  from  the  Pulse  as  to 
the  Nature  and  Extent  of  Valvular  Lesion. 

In  aortic  stenosis  the  artery  will  be  somewhat  small,  and 
full  between  the  beats  ;  the  initial  percussion-wave  will  be 
slight  and  gradual,  and  the  pulse-wave  prolonged.  This 
modification  of  the  pulse  is  due  to  the  fact  that  the  blood 
has  to  pass  through  a  narrowed  orifice  on  its  way  from  the 
left  ventricle  into  the  aorta.  Hence  the  impact  of  the 
systole  upon  the  column  of  blood  in  the  aorta  will  be 
diminished,  and  more  time  will  be  required  for  the  passage 
of  the  contents  of  the  ventricle  into  the  arterial  system. 

In  aortic  incompetence  we  have  the  well-known  collapsing 
or  water-hammer  pulse ;  the  artery  is  large,  and  empty 
between  the  beats ;  the  pulse-wave  is  sudden,  forcible,  short, 
and  ill-sustained,  and  its  cessation  is  very  abrupt. 

In  mitral  stenosis  the  artery  is  small,  full  between  the 
beats,  with  higher  tension  than  would  be  expected,  and  the 
pulse-wave  is  long. 

In  all  these  three  forms  of  valve-lesion  the  pulse  is 
regular  till  the  heart  begins  to  break  down. 

In  mitral  regurgitation,  on  the  other  hand,  the  pulse  is 
usually  irregular,  both  in  force  and  frecpuency,  if  the  lesion 


THE  PULSE   IN   VALVULAR   LESIONS.  97 

is  at  all  severe.     The  pulse-wave  is  also  short,  and  passes 
the  finger  rapidly. 

The  characteristics  of  the  different  types  of  pulse,  as 
brought  out  by  the  sphygmograph,  are  shown  in  the  accom- 
panying tracings. 


FIG.  11. — AOKTIC  STENOSIS. 


FIG.  12. AOKTIC    INCOMPETENCE. 


FIG.    13. — MITRAL    STENOSIS. 


FIG     14. — MITRAL   INCOMPETENCE. 

In  Fig.  11,  the  pulse  of  aortic  stenosis,  it  will  be  seen 
that  the  wave  is  of  little  altitude,  and  has  a  sloping 
upstroke,  with  a  rounded  top  and  a  gradual  descent ;  that 
is  to  say,  the  wave  is  small,  and  attains  its  maximum 
gradually,  is  persistent  or  long,  and  subsides  slowly.     There 

H 


98  HEART  DISEASE. 

is  no  dicrotic  wave,  as  the  conditions  necessary  for  its  pro- 
duction, great  fluctuation  of  the  blood-pressure  and  rapid 
contraction  of  the  ventricle,  are  absent. 

In  Fig.  12,  the  pulse  of  aortic  incompetence,  the  upstroke 
is  high,  perpendicular,  has  a  sharp  top,  and  falls  rapidly ; 
that  is,  the  wave  is  large,  owing  to  the  size  of  the  artery, 
is  sudden  and  rapidly  attains  its  maximum,  is  very  short 
and  rapidly  falls.  Dicrotism  is  not  altogether  absent,  but, 
owing  to  want  of  the  fulcrum  formed  by  the  aortic  valves, 
it  is  much  less  marked  than  might  be  exj)ected  from  the 
violence  of  the  fluctuations  and  the  rapidity  of  the  systole. 

In  Fig.  13,  the  pulse  of  mitral  stenosis,  the  upstroke  or 
percussion-wave  is  short,  and  soon  attains  its  maximum ; 
the  wave  is  long,  and  is  slowly  extinguished.  Dicrotism 
is  absent. 

In  Fig.  14,  the  pulse  of  severe  mitral  incompetence,  the 
tracing  shows  that  the  pulse  is  very  irregular  both  in  force 
and  frequency ;  the  wave  is  short  and  small,  and  ill-sustained. 
When,  however,  the  amount  of  regurgitation  is  slight  and 
compensation  is  good,  the  pulse  will  usually  be  regular. 

The  character  of  the  pulse,  therefore,  affords  important 
information  as  to  the  nature  of  the  lesion  ;  while  the  degree 
in  which  the  special  peculiarities  are  developed,  in  each 
instance  gives  some  clue  to  the  extent  of  the  valvular 
mischief.  The  pulse,  however,  may  be  modified  in  various 
ways;  for  instance,  where  aortic  stenosis  co-exists  with 
regurgitation,  the  collapsing  and  sudden  character  of  the 
regurgitant  pulse  will,  to  a  great  extent,  be  lost.  Such 
modification,  when  present,  is  in  itself  a  valuable  help  to 
diagnosis,  as  it  enables  us  to  say  with  certainty  that  there 
is  real  aortic  stenosis,  and  not  merely  roughening  of  the 
aortic  valves,  either  of  which  might  be  indicated  by  the 
presence  of  a  systolic  basic  murmur. 

Much  information  may  thus  be  gained  from  the  pulse ; 
but    the    character    of    the    pulse,    even    when    taken    in 


THE  PULSE  IN  VALVULAR  LESIONS.  99 

connection  with  the  murmurs,  is  not  sufficient  to  enable 
us  to  estimate  the  degree  of  obstruction  or  the  amount  of 
regurgitation  in  a  given  case.  Further  indications  are  to 
be  obtained,  firstly,  from  the  effects  on  the  cavities  and 
walls  of  the  heart  produced  by  the  mechanical  difficulties 
resulting  from  the  valvular  imperfections  ;  secondly,  from 
the  evidences  of  obstructed  circulation  in  the  lungs  or 
system. 


CHAPTEK  VIII. 

THE  IMPOETANCE  OP  HYPEETEOPHY  AND  DILATATION  OF 
THE  HEAKT  AS  A  MEANS  OF  ESTIMATING  THE  EXTENT 
OF  A  VALVULAE  LESION — POSSIBLE  OBJECTIONS  TO  THIS 
VIEW  DISCUSSED— EXPLANATION  OF  THE  WAY  IN  WHICH 
THE  DIFFEEENT  VALVULAE  LESIONS  GIVE  EISE  TO 
HYPEETEOPHY  AND  DILATATION  :  (1)  AOETIC  STENOSIS  ; 
(2)  AOETIC  INCOMPETENCE  ;  (3)  MITEAL  EEGUEGITA- 
TION;    (4)  MITEAL   OBSTEUCTION — COMPENSATION. 

The  most  important  indications  as  to  the  extent  of  a 
valvular  lesion  are  to  be  gathered  from  its  effects  on  the 
walls  and  cavities  of  the  heart,  resulting  in  hypertrophy  of 
the  former  and  dilatation  of  the  latter.  These  changes  are 
due  to  the  efforts  of  the  heart  to  overcome  the  mechanical 
difficulties  in  the  circulation  occasioned  by  the  regurgitation 
or  obstruction  to  which  the  valvular  lesion  has  given  rise. 

Hypertrophy  and  dilatation  must  be  looked  upon  as 
caused  by  the  valvular  lesion,  and  as  affording  a  measure 
of  its  extent.  The  degree  of  these  structural  changes  is 
ascertained  by  the  increased  area  of  deep  cardiac  dulness, 
by  the  displacement  and  modification  of  the  apex  beat,  by 
the  situation  and  character  of  the  impulse,  and  by  associated 
changes  in  the  character  and  rhythm  of  the  heart-sounds ; 
the  more  pronounced  these  changes,  the  greater  is  the 
mechanical  difficulty  in  the  propulsion  of  the  blood,  and  the 
more  grave  is  the  prognosis. 

Not  that  a  given  degree  of  hypertrophy  or  dilatation, 


IlYPERTROriTY  AND  DILATATION  OF  THE  HEART.      101 

or  of  the  two  combined,  is  indicative  in  all  cases  of  the 
same  extent  of  valvular  change.  Each  kind  of  valvular 
disease  has  its  own  special  form  and  degree  of  structural 
change,  and  comparisons,  to  be  valid,  must  be  made  between 
like  cases  ;  a  degree  of  hypertrophy  and  dilatation,  which 
would  have  little  significance  in  aortic  insufficiency,  might 
indicate  a  serious  amount  of  mitral  regurgitation ;  and 
again,  mitral  stenosis,  which  has  reached  a  dangerous 
degree,  may  be  attended  with  less  conspicuous  structural 
change  than  a  degree  of  mitral  insufficiency  which  gives 
rise  neither  to  danger  nor  to  inconvenience.  It  will  be 
well,  indeed,  to  exclude  mitral  stenosis  while  the  general 
question  under  consideration  is  argued  out.  Numerous 
other  modifying  influences  are  also  in  operation,  so  that, 
while  it  is  generally  true  that  the  greater  the  dilatation  and 
hypertrophy,  the  greater  the  functional  imperfection  of  the 
valves,  the  converse  statement,  that  the  less  the  hypertrophy 
or  dilatation,  the  smaller  the  valvular  damage,  must  not  be 
taken  without  important  qualifications.  This  statement  is 
indeed  usually  true  in  the  absence  of  serious  symptoms,  but 
sometimes  the  very  failure  of  the  heart  to  undergo  the 
changes  required  for  the  compensation  of  valvular  in- 
efficiency causes  severe  embarrassment  of  the  circulation, 
and  gives  rise  to  an  early  fatal  termination. 

It  is  stated  by  Walshe,  and  is  undoubtedly  true,  that  no 
direct  ratio  constantly  holds  good  between  the  amount  of 
hypertrophy  and  valvular  change,  as  ascertained  by  post- 
mortem examinations.  This,  however,  is  capable  of  explana- 
tion, if  we  take  into  account  the  various  circumstances  that 
may  modify  the  development  of  the  hypertrophy. 

Firstly.  The  age  of  the  patient  at  the  time  when  the 
lesions  of  the  valves  take  place  is  an  important  factor.  The 
enormous  hypertrophy  and  dilatation  sometimes  met  with 
are  produced  almost  exclusively  in  early  life,  when  the 
heart   is   still   developing   and   its   muscular   substance  is 


io2  HEART  DISEASE. 

capable  of  active  growth ;  later,  trie  heart  loses  its  adaptive 
capability  in  great  measure,  and  thus  a  valvular  lesion 
which,  at  the  age  of  fifteen  or  twenty,  would  be  survived 
with  enormous  hypertrophy,  would  at  forty  or  fifty  prove 
fatal  with  very  little  change. 

Secondly.  Time  is  an  important  element  in  the  develop- 
ment of  hypertrophy,  which  may  take  years  to  reach  its 
maximum  growth  ;  and  it  is  often  very  difficult  to  assign 
a  date  to  the  origin  of  a  given  morbid  condition.  For 
instance,  of  two  cases  in  which  the  extent  of  the  valvular 
mischief,  as  seen  by  post-mortem,  is  apparently  the  same, 
in  one  the  heart  may  be  found  to  be  considerably  hyper- 
trophied,  because  the  patient  did  not  at  once  succumb  to 
the  injury  ;  in  the  other  there  is  perhaps  little  hypertrophy 
but  great  dilatation,  because  the  difficulty  of  carrying  on 
the  circulation  increased  more  rapidly  than  the  power  of  the 
heart  to  cope  with  it,  so  that  death  occurred  quickly. 

Thirdly.  We  must  take  into  account  the  fact  that 
different  affections  of  the  valves  have  inherently  and 
mechanically  different  degrees  of  tendency  to  the  pro- 
duction of  structural  alterations.  For  instance,  aortic  in- 
competence gives  rise  to  enormous  hypertrophy  of  the  left 
ventricle,  whereas  mitral  incompetence  gives  rise  to  very 
moderate  hypertrophy,  and  uncomplicated  mitral  stenosis 
to  atrophy  rather  than  hypertrophy. 

Fourthly.  The  mode  of  life,  whether  active  and  accom- 
panied by  considerable  muscular  exertion,  or  sedentary  and 
unattended  by  anxiety  and  excitement,  will  be  an  important 
consideration.  The  amount  of  work  the  heart  is  called  upon 
to  do  will  vary  in  each  instance,  and  the  hypertrophy  will 
vary  in  direct  proportion. 

Again,  the  presence  of  high  tension  in  the  vascular 
system  will  tend  to  increase  the  degree  of  hypertrophy  to 
a  considerable  extent. 

Fifthly.     The  period  after  the  occurrence  of  the  valvular 


HYPERTROPHY  AND  DILATATION  OF  THE   HEART.      103 

change  at  which  active  exertion  is  undertaken,  allowing  or 
not  allowing  the  heart  to  adapt  itself  gradually  to  this 
change,  will  have  great  influence  on  the  condition  of  its 
walls  and  cavities.  For  example,  after  endocarditis,  which 
has  given  rise  to  damage  of  the  aortic  or  mitral  valve,  one 
patient  has  prolonged  rest,  care,  comforts,  and  change  of  air, 
so  that  dilating  influences  are  postponed  by  the  rest  while 
the  heart  is  weak  and  liable  to  yield,  and  the  muscular 
walls  are  enabled,  by  a  good  state  of  nutrition,  to  resist 
dilatation ;  another  must  return  to  work,  or  is  allowed  to 
exert  himself  before  the  heart  has  recovered  from  the  effects 
of  the  illness,  and  its  badly  nourished  fibres  give  way  and 
permit  of  dilatation,  which  will  be  followed  later,  if  the 
patient  lives,  by  hypertrophy. 

We  have  in  the  above  conditions  the  quota  of  causation, 
beyond  the  mechanical  difficulty  at  the  valves,  which 
explains  the  variation  observed ;  and  it  will  be  evident, 
from  these  considerations,  that  an  unvarying  direct  ratio 
between  the  valvular  and  structural  changes  is  not  to 
be  looked  for,  and  that  its  absence  furnishes  no  valid 
objection  to  their  standing  in  the  relation  of  cause  and 
effect. 


Mechanism    of    Causation   op    Hypeeteophy    in   the 
dlffebent    valvulae    diseases  :    its    beneficial 

Effects. 

Aortic  Stenosis. — Taking  first  the  most  simple  case.  If 
the  constriction  of  the  aortic  orifice  is  sufficient  in  amount 
to  give  rise  to  mechanical  obstruction  to  the  flow  of  blood 
through  it,  there  must  either  be  increase  in  the  propulsive 
power  of  the  heart,  or  a  slowing  of  the  circulation  ;  for  it 
is  obvious  that  the  same  force  will  not  propel  the  same 
amount  of  blood  in  the  same  time  through  a  narrowed 
orifice  as  through  one  of  normal   size.     We  find,  however. 


io4  HEART  DISEASE. 

that  the  rate  of  circulation  is  maintained,  the  increased 
power  necessary  to  drive  the  blood  through  the  narrowed 
orifice  at  a  more  rapid  rate  being  gained  by  hypertrophy 
of  the  heart,  which  takes  place  to  a  degree  necessary  to 
overcome  the  obstruction.  This  is  a  simple  illustration  of  the 
physiological  law,  that  increased  functional  activity  gives 
rise  to  increase  of  structure.  If  the  hypertrophy  did  not 
take  place,  there  would  be  a  slowing  and  finally  a  standstill 
of  the  circulation. 

Aortic  Insufficiency. — In  this  lesion  a  certain  proportion 
of  the  blood  driven  into  the  aorta  at  each  systole  returns 
into  the  ventricle  through  the  leaking  valves ;  conse- 
quently, in  order  that  the  same  rate  of  circulation  may  be 
maintained,  there  must  be  either  an  increase  in  the  number 
of  heart-beats  per  minute,  or  an  increase  in  the  quantity  of 
blood  expelled  by  the  ventricle  at  each  contraction.  Mere 
augmentation  of  the  force  of  the  systole  would  not  answer 
the  requirement :  for  instance,  if  five  ounces  of  blood  are 
driven  into  the  aorta  at  each  systole,  and  one  ounce  re- 
turns, the  normal,  supply  of  blood  would  obviously  not  be 
maintained  by  propelling  the  five  ounces  more  forcibly  ; 
what  is  needed  is  that  six  ounces  of  blood  should  be  driven 
into  the  aorta,  so  that  when  one  ounce  has  regurgitated 
into  the  ventricle,  five  ounces  would  still  remain  in  the 
arterial  system.  This  requirement  is  met  by  an  increased 
capacity  of  the  left  ventricle,  which  is  the  primary  com- 
pensatory change  taking  place  in  aortic  insufficiency. 
Increased  capacity  is,  in  other  words,  dilatation.  In  this 
instance,  therefore,  dilatation  of  the  left  ventricle,  which 
under  other  conditions  is  injurious,  is  actually  a  beneficial 
and  conservative  change  when  reinforced  by  hypertrophy, 
and  this  we  shall  see  is  a  natural  sequence. 

It  is  true  there  is  no  direct  provocation  to  hypertrophy  in 
the  shape  of  increased  resistance  to  the  blood-flow  ;  but  there 
is  a  call    for  increased    exercise  of  force  in  the  additional 


HYPERTROPHY  AND   DILATATION  OF  THE   HEART.      105 

quantity  of  blood  to  be  projected  from  the  ventricle  into 
the  aorta  at  each  systole.  Further,  the  total  internal  area 
of  the  walls  of  the  ventricle  is  greatly  increased  owing 
to  the  increase  in  its  capacity,  while  the  same  pressure  is 
exerted  on  each  square  inch  during  systole,  hence  the 
amount  of  force  to  be  exercised  by  the  muscular  walls  of 
the  heart  must  be  proportionately  augmented.  These  two 
causes  give  rise  to  the  hypertrophy  present  in  so  remark- 
able a  degree  in  aortic  regurgitation. 

It  must  not  be  supposed  that,  because  the  dilatation  which 
takes  place  in  aortic  regurgitation  is  compensatory  and 
necessary,  this  is  a  sufficient  explanation  of  its  occurrence. 
It  is  produced  in  the  following  way  :  During  diastole,  the 
most  defenceless  period  of  the  heart  in  the  cardiac  cycle, 
when  the  muscular  fibres  are  in  a  state  of  relaxation,  the 
ventricle  is  exposed  to  a  double  distending  force.  Firstly, 
the  entry  of  blood  from  the  left  auricle  and  pulmonary 
veins ;  secondly,  the  backward  rush  of  the  blood  from  the 
aorta:  the  greater  the  amount  of  the  regurgitation,  the 
greater  will  be  the  distending  force,  and  consequently 
the  greater  the  dilatation  of  the  left  ventricle.  This  dila- 
tation, however,  is  a  totally  different  thing  from  the  dilata- 
tion which  is  sometimes  met  with  as  the  result  of  structural 
change  and  degeneracy  of  the  muscular  walls  of  the  heart : 
in  the  latter  case,  the  walls  yield  because  they  are  in- 
herently weak,  and  the  effect  on  the  circulation  is  dis- 
astrous, a  gradually  increasing  stagnation  from  deficient 
vis  a  tergo ;  in  the  former  case  the  walls  yield,  not  because 
they  are  weak,  but  because  they  are  subjected  to  an 
abnormal  distending  force  while  in  a  condition  of  relaxation 
and  least  able  to  resist  it ;  ultimately,  when  this  dilatation 
is  backed  by  hypertrophy,  the  effect  on  the  circulation  ig 
beneficial,  since  it  neutralizes,  more  or  less  completely,  the 
tendency  to  stagnation  produced  by  the  regurgitation. 

When,  however,  aortic  regurgitant  disease  is  set  up  late 


ro6  HEART  DISEASE. 

in  life  from  degenerative  changes  in  the  valves,  there  is 
frequently  also  degeneration  and  consequent  weakening  of 
the  muscular  substance  of  the  heart ;  then,  owing  to  the 
inherent  weakness  of  the  walls  of  the  heart,  the  dilatation 
due  to  the  aortic  regurgitation  will  be  excessive,  unless 
the  case  is  cut  short  by  sudden  death,  and,  as  there  is 
little  chance  of  sufficient  compensatory  hypertrophy  taking 
place,  the  condition  will  be  one  of  distress  and  danger,  if 
the  regurgitation  is  extensive. 


MlTKAL   BeGURGITATION   AND   MlTRAL    OBSTRUCTION. 

In  affections  of  the  mitral  valve  the  effects  of  the 
derangement  of  the  circulation  due  to  the  lesion  no  longer 
fall  mainly  on  the  left  ventricle,  but  primarily  on  the  left 
auricle  and  lungs,  and  eventually  on  the  right  ventricle. 
The  left  auricle  in  mitral  lesions  corresponds  in  its  relation 
to  the  current  of  blood  to  the  left  ventricle  in  aortic  lesions  ; 
hence,  by  analogy,  in  mitral  regurgitation,  we  should  expect 
to  find  hypertrophy  and  dilatation,  and  in  mitral  obstruction 
marked  hypertrophy  of  the  left  auricle.  This  is  what  occurs 
to  a  certain  extent,  but  as  the  auricle  is  thin  walled  and 
poor  in  muscular  substance,  it  is  impossible  for  it  to  take 
on  hypertrophy  and  compensate  for  the  mitral  lesions  in 
the  same  way  that  the  ventricle  does  for  aortic  lesions; 
it  may,  indeed,  be  distended  so  as  to  form  a  thin  walled 
sac  of  considerable  size.  The  result  is  that  the  burden  of 
the  work  of  compensation  is  thrown  on  the  right  ventricle 
by  back  pressure  through  the  pulmonary  circulation,  which 
thus  becomes  the  channel  through  which  the  effects  of  the 
mitral  regurgitation  or  obstruction  are  transmitted  from  the 
left  auricle  to  the  right  ventricle.  We  find,  therefore, 
that  the  right  ventricle  undergoes  hypertrophy  and  dila- 
tation  as  a  result    of  mitral   lesions,    while    the    pressure 


HYPERTROPHY  AND  DILATATION  OF  THE  HEART      107 

in  the  pulmonary  circulation,  the  connecting  channel,  is 
enormously  increased. 

It  thus  comes  to  pass  that  the  right  ventricle,  by  the 
additional  force  it  gains  from  hypertrophy  and  the  ad- 
ditional capacity  it  gains  from  dilatation,  aids  in  supplying 
the  left  ventricle  with  blood,  and  in  neutralizing  the  dis- 
turbing effects  of  mitral  lesions  on  the  circulation ;  for  the 
increased  pressure  in  the  pulmonary  system  and  left  auricle 
will  send  the  blood  more  rapidly  through  a  constricted 
orifice  in  case  of  mitral  stenosis,  and  will  resist  the  regur- 
itation  in  mitral  incompetence. 

Dilatation  of  the  Left  Venteicle  in  Miteal 
Incompetence. 

A  certain  limited  amount  of  dilatation  and  hypertrophy 
of  the  left  ventricle,  as  well  as  of  the  right,  takes  place 
in  mitral  incompetence,  the  explanation  of  which  is  as 
follows  : — 

During  diastole,  in  consequence  of  the  increased  pressure 
in  the  pulmonary  circulation  and  left  auricle,  the  blood 
will  rush  through  the  mitral  orifice  with  greater  force  and 
rapidity  than  normal ;  hence  the  pressure  on  the  walls  of 
the  left  ventricle  will  be  greater  than  normal,  and  the 
muscular  fibres,  being  relaxed  and  defenceless,  readily  yield 
to  the  extra  distending  force  :  in  this  way  some  degree  of 
dilatation  results.  Then  as  the  dilatation  increases  the 
area  of  ventricular  wall  exposed  to  pressure,  it  increases 
also  the  amount  of  work  to  be  done  in  systole,  and  thus 
creates  a  demand  for  hypertrophy,  which  also  takes  place 
to  a  moderate  extent. 

In  mitral  stenosis,  though  there  is  increased  pressure 
in  the  pulmonary  circulation  which  would  tend  to  cause 
dilatation  of  the  left  ventricle  during  diastole  in  the  same 
way  as   in  mitral   incompetence,  the  mitral  orifice,  being 


ioS  HEART  DISEASE. 

narrowed,  does  not  allow  a  volume  of  blood,  sufficient  to 
exert  a  distending  force,  to  pass  through ;  indeed,  in  severe 
cases,  the  constriction  may  be  so  great  that  the  ventricle 
has  never  time  to  fill  during  diastole,  so  that  it  tends  rather 
to  decrease  in  size  than  dilate,  and  there  will  be  no  demand 
for  hypertrophy. 

In  incompetence  of  the  mitral  valve,  therefore,  the  amount 
of  hypertrophy  and  dilatation  of  the  right  ventricle  and 
the  degree  of  pressure  in  the  pulmonary  circulation  are 
among  the  most  important  indications  of  the  extent  of  the 
lesion. 

In  mitral  stenosis  this  holds  good  up  to  a  certain  point, 
but  the  changes  in  the  right  ventricle  are  not  so  safe  a 
guide,  since  the  dilatation  and  hypertrophy  sometimes 
appear  to  be  restricted  in  extent  by  the  absence  of  accom- 
panying changes  of  a  similar  character  in  the  left  ventricle, 
which  remains  very  small. 

Compensation. 

It  has  thus  been  seen  that  dilatation  and  hypertrophy 
of  the  left  or  right  ventricle  or  of  both  are  a  necessary 
consequence  of  valvular  disease  of  any  severity,  if  the 
patient  lives,  and  the  mechanism  of  their  production  has 
also  been  discussed.  These  changes  in  the  cardiac  walls 
are  spoken  of  as  compensatory,  that  is,  they  are  changes 
which  must  take  place  to  enable  the  heart  to  cope  with 
the  extra  work  thrown  upon  it  as  a  result  of  the  valvular 
lesions  ;  in  the  case  of  aortic  disease  it  is  the  left  ventricles 
in  the  case  of  mitral  lesions  the  right  ventricle,  more 
especially,  which  undergoes  compensatory  changes.  Com- 
pensation is  said  to  be  established  when  the  hypertrophy 
and  dilatation,  the  former  especially,  have  so  far  developed 
that  they  neutralize  the  disturbing  effects  on  the  circulation 
which  the  valvular  lesions  would  otherwise   produce,  and 


COMPENSATION.  109 

enable  the  patient  to  live  his  ordinary  life  without  dis- 
comfort, and  without  any  marked  symptoms. 

When  compensation  is  imperfect,  the  symptoms  incident 
to  the  valvular  disease  from  which  the  patient  is  suffering 
will  present  themselves  more  or  less  readily  under  moderate 
exercise  or  exertion,  their  severity  varying  inversely  with 
the  degree  of  compensation  established. 

For  instance,  a  boy  who  is  allowed  to  go  about  imme- 
diately after  he  has  contracted  a  valvular  lesion  of  some 
severity,  and  is  suffering,  say,  from  aortic  incompetence, 
will  be  extremely  short  of  breath,  and  incapable  of  walking 
any  distance,  will  have  attacks  of  severe  pain  in  the  pra3- 
cordium,  and  perhaps  fainting  fits,  one  of  which  may  prove 
fatal ;  whereas  the  same  patient,  if  he  is  kept  at  rest  till  the 
compensatory  changes  have  had  time  to  develop,  will  be 
able  to  take  moderate  exercise  comfortably  and  go  about 
his  work  free  from  pain  or  respiratory  distress,  though  he 
may  be  incapable  of  any  prolonged  or  violent  exertion. 

In  mitral  disease  dyspnoea,  cyanosis,  and  oedema  of  the 
lower  extremities  are  among  the  earlier  symptoms  of  failing 
compensation.  In  the  later  stages  one  of  the  most  impor- 
tant guides  as  to  the  state  of  compensation  is  the  size  of  the 
liver.  When  this  organ  becomes  engorged  and  enlarged, 
owing  to  obstruction  to  the  flow  of  blood  from  the  inferior 
vena  cava  to  the  right  auricle,  it  will  indicate  that  the 
right  ventricle  is  unable  to  cope  efficiently  with  the  in- 
creased pressure  in  the  pulmonary  circulation  caused  by 
the  mitral  lesion,  and  consequently  that  compensation  is 
imperfect.  A  further  indication  will  be  pulsation  and 
fulness  of  the  veins  of  the  neck,  which  may  sometimes  be 
seen  to  fill  from  below.  The  liver  may  attain  a  consider- 
able size,  extending  below  the  umbilicus,  and  may  even- 
tually pulsate  when  tricuspid  regurgitation  has  become 
established. 


CHAPTER  IX. 
AORTIC   STENOSIS. 

MORBID  ANATOMY  AND  ETIOLOGY — THE  MURMUR  OF  AORTIC 
STENOSIS— CONDITIONS  OTHER  THAN  AORTIC  STENOSIS 
WHICH  MAY  GIVE  RISE  TO  SYSTOLIC  AORTIC  MURMURS 
— DIFFERENTIAL  DIAGNOSIS  OF  MURMURS — ESTIMATION 
OF  EXTENT  OF  LESION  BY  MEANS  OF  THE  MURMUR, 
THE  CHANGES  IN  THE  HEART  AND  THE  PULSE — 
PROGRESS  OF  THE  DISEASE  :  SYMPTOMS— PROGNOSIS — 
TREATMENT. 

The  first  valvular  change  to  be  considered  will  be  aortic 
stenosis.  This  is  the  least  common  of  the  valvular  affections 
of  the  left  side  of  the  heart,  as  shown  both  by  post-mortem 
statistics  and  clinical  experience. 

Morbid  Anatomy  and  Etiology. 

Actual  narrowing  of  the  mouth  of  the  aorta  is  almost 
always  due  to  changes  in  the  valves,  the  cusps  of  which 
may  be  stiff  and  rigid  from  cicatricial  contraction  of  fibrous 
tissue  after  endocarditis,  with  rounded  and  thickened 
margins,  a  condition  which  does  not  permit  them  to  fall 
back  into  the  sinuses  of  Valsalva  before  the  current  of 
blood.  Instead,  therefore,  of  a  circular  orifice  of  the  same 
size  as  the  vessel  beyond,  there  is  a  roughly  triangular 
opening  of  reduced  area,  formed  by  the  edges  of  the 
cusps :    subsequent    calcification    may    render    the    valves 


AORTIC  STENOSIS.  in 

still  more  rigid  and  deformed.  Sometimes  adhesions  take 
place  between  damaged  valves  at  the  angle  in  which  they 
meet,  so  that  a  narrow  funnel-shaped  orifice  results.  This 
condition  may  be  left  by  endocarditis,  whether  rheumatic 
or  occurring  in  the  course  of  scarlet  fever  or  other  bacterial, 
infection  of  the  valves.  Or  the  valves  may  be  deformed 
by  atheroma  or  chronic  degenerative  changes,  which  destroy 
their  flexibility,  cause  puckering  and  contraction  of  their 
margins,  and  lead  to  calcareous  deposits  in  their  substance. 

It  is  also  possible  that  by  dilatation  of  the  ring  at  the 
root  of  the  aorta,  a  slight  and  unimportant  obstruction  may 
be  produced  ;  valves,  not  themselves  greatly  diseased,  being 
so  put  on  the  stretch  that  they  cannot  fall  back,  but  remain 
as  an  obstacle  to  the  stream  of  blood. 

Physical  Signs. 

The  characteristic  physical  sign  to  which  aortic  stenosis 
gives  rise  is  a  murmur  systolic  in  time  which  usually  has 
its  maximum  intensity  in  the  second  right  intercostal  space 
close  to  the  sternum,  in  the  so-called  aortic  area.  All 
systolic  murmurs  heard  over  this  area  do  not,  however, 
necessarily  imply  actual  obstruction  of  the  aortic  orifice, 
but  may  have  other  significance. 

The  Murmur. — The  systolic  aortic  murmur,  as  is  indicated 
by  its  name,  is  heard  during  the  systole  of  the  left  ventricle, 
and  is  produced  by  the  rush  of  blood  through  the  obstructed 
aortic  orifice  from  the  ventricle  into  the  aorta.  Its 
commencement  coincides  in  time  with  the  first  sound 
of  the  heart,  and  may  either  accompany  or  replace  it, 
and  it  may  begin  with  a  burst  or  accent,  or  gradually. 
The  duration  of  the  murmur  varies  ;  it  is  usually  long, 
sometimes  occupying  the  entire  interval  between  the  first 
and  second  sounds,  which  interval  may  be  prolonged,  but  it 
may  be  short.  It  is  audible  over  the  sternum  at  the  level 
of  the   third   intercostal   space,  but   is   most  distinct  just 


U2  HEART  DISEASE. 

outside  the  right  edge  of  the  sternum  in  the  second  space, 
or  sometimes  over  the  third  costal  cartilage,  at  which  point 
on  the  surface  the  aorta  comes  from  under  the  pulmonary 
artery,  and  nearly  touches  the  anterior  wall  of  the  chest. 
It  is  conducted  upwards,  as  the  phrase  is,  along  the  right 
side  of  the  sternum  to  the  right  sterno-clavicular  articu- 
lation, where  it  is  distinctly  audible,  and  it  is  also  heard 
over  the  carotids  in  the  neck  and  occasionally  over  the 
thoracic  aorta  along  the  spine.  It  is  frequently  heard  along 
the  right  margin  of  the  sternum  lower  down,  sometimes 
to  the  fourth  or  fifth  space  right  or  left  of  the  sternum, 
more  especially  when  the  aorta  is  dilated  and  elon- 
gated, and  it  may  have  its  maximum  intensity  over  the 
sternum  near  its  left  edge  at  the  level  of  the  third  rib  or 
space,  i.e.  immediately  over  the  aortic  valves.  This,  however, 
is  not  common,  as  the  root  of  the  aorta  is  deeply  seated  in 
the  chest,  and  has,  between  it  and  the  surface,  the  conus 
arteriosus  of  the  pulmonary  artery.  The  murmur  is  lost 
over  the  right  ventricle,  but  is  again  audible,  as  a  rule,  at 
the  apex,  being  conducted  to  this  point  by  the  wall  of  the 
left  ventricle.  This  murmur  may  be  loud — sometimes 
extremely  loud — and  when  this  is  the  case,  it  may  be  heard 
all  over  the  chest  behind,  as  well  as  in  front,  or  it  may  be 
comparatively  soft ;  it  is  often  rough  and  vibratory,  more 
rarely,  croaking  in  character,  but  it  may  be  smooth  and 
blowing,  or  musical.  Occasionally  it  is  accompanied  by  a 
systolic  thrill  felt  in  the  second  or  third  right  space,  or  in 
both  close  to  the  edge  of  the  sternum. 

Causes  other  than  Aortic  Stenosis  which  may  give  rise  to 
a  Basic  Systolic  Murmur. — Such  a  murmur  in  one  or  other 
of  its  varieties  may  be  due  to  several  causes,  which  will 
now  be  enumerated. 

1.  Anaemia  may  be  mentioned  first.  It  is  not  well 
understood  how  it  is  that  this  condition  gives  rise  to 
murmurs,  but  the  fact  is  exemplified  by  the  venous  hum 


AORTIC  STENOSIS.  113 

heard  in  the  neck,  by  pulmonic  and  mitral  murmurs,  and 
also,  though  less  commonly,  by  a  systolic  aortic  murmur. 
This  murmur  is  rarely  rough  or  loud,  but  it  is  often  distinct 
and  audible  along  the  edge  of  the  sternum  upwards  to  the 
sterno-clavicular  articulation,  and  in  the  neck.  It  accom- 
panies the  first  sound,  and  does  not  substitute  itself  for  it. 
Haemic  murmurs  are  commonly  multiple,  which  renders 
their  diagnosis  more  easy. 

With  the  uremic  aortic  murmur  may  be  grouped  the 
murmur  of  similar  character,  sometimes  accompanying  or 
following  acute  febrile  disease  of  long  duration,  such  as 
rheumatic  fever  and  typhoid  fever,  although  it  is  not  certain 
that  the  causation  is  exactly  the  same.  A  systolic  mitral 
murmur  is  more  common,  and  is  usually  present  as  well  as 
the  aortic  murmur.  Such  murmurs  may  perhaps  be  attri- 
buted to  a  temporary  loss  of  tone  of  the  heart  and  vessels. 
They  usually  disappear  as  the  patient  regains  health  and 
strength. 

2.  Mere  roughening  of  the  orifice  or  valves,  or  impaired 
flexibility  of  the  latter,  slight  congenital  malformation, 
fenestration  of  one  or  more  of  the  cusps,  a  shred  of  fibrin 
hanging  from  the  edge  of  a  valve,  may  give  rise  to  a  loud 
systolic  murmur  without  offering  any  appreciable  obstruc- 
tion to  the  course  of  the  blood. 

3.  An  aortic  murmur  may  be  produced  by  acute  or  sub- 
acute aortitis,  a  rare  and  obscure  disease  which  may  be 
suspected  when,  with  a  murmur  not  previously  known  to  be 
present,  there  are  irregular  pyrexia,  dull  sub-sternal  pain, 
and  rapid  and  apparently  unaccountable  failure  of  the  heart. 

4.  Dilatation  of  the  aorta  just  above  the  valves,  the 
orifice  and  valves  remaining  unchanged,  produces  a  murmur. 
The  fibrous  ring  at  the  root  of  the  aorta,  which  gives  attach- 
ment to  the  muscular  fibres  of  the  ventricle,  and  supports 
the  semilunar  valves,  is  extremely  strong,  so  that  it  does 
not  readily  give  way  and  allow  the  orifice  to  be  enlarged, 

1 


H4  HEART  DISEASE. 

but  the  aorta  just  above  the  ring  is  prone  to  dilatation,  and 
the  blood  passing-  through  an  opening  of  normal  size  into  a 
larger  cavity  beyond  is  thrown  into  eddies,  the  vibrations 
attending  which  produce  the  sound  heard  as  a  murmur. 

In  none  of  these  conditions  is  there  stenosis  of  the 
orifice,  or  obstruction  to  the  stream  as  it  issues  from  the 
heart ;  the  condition  last  mentioned  has  dangers  of  its  own, 
but  they  do  not  arise  from  aortic  obstruction. 

Differential  Diagnosis  of  Basic  Systolic  Murmurs. — It 
is  clear  that  the  first  point  to  be  ascertained  when  a 
systolic  murmur  is  present  is,  whether  it  indicates  the 
existence  of  obstruction  or  not.  In  this  we  shall  be  greatly 
assisted  by  the  history,  aspect,  and  age  of  the  patient. 
We  should,  for  example,  suspect  that  the  murmur  was 
hsemiCj  and  not  produced  by  obstruction  if  the  patient 
were  a  young  and  ansemic  girl,  or  if  it  were  first  heard 
during  convalescence  from  an  acute  illness,  more  especially  if 
similar  blowing  murmurs  were  heard  at  other  valves  as  well. 

The  history  of  an  attack  of  rheumatic  fever  would,  on 
the  other  hand,  favour  the  conclusion  that  the  orifice  was 
actually  narrowed. 

A  systolic  murmur  over  the  aorta,  appearing  after  middle 
age,  or  in  advanced  life,  or  discovered  for  the  first  time  at 
this  period,  will  seldom  be  due  to  actual  narrowing  of  the 
orifice,  but  will  be  caused  by  roughness  or  rigidity  of  the 
valves,  or  by  dilatation  of  the  aorta  above  the  valves  with 
perhaps  atheromatous  irregularities  in  its  walls.  Fortu- 
nately the  aortic  second  sound  is  of  very  great  assistance 
in  determining  the  point.  Under  the  condition  just 
mentioned  it  will  almost  certainly  be  unduly  loud  and 
accentuated  from  co-existing  high  arterial  tension,  while 
stenosis  diminishes  the  intensity  of  the  second  sound  in  two 
ways  :  by  the  changes  present  in  the  valves  impairing  their 
flexibility,  and  by  the  less  sudden  recoil  which  follows 
the   slower   distension  of  the   arterial  system.     Prolonged 


AORTIC   STENOSIS.  115 

observation  of  cases  of  high  arterial  tension  from  gout,  lead 
poisoning,  renal  disease,  or  other  causes  in  advanced  life, 
will  not  unfrequently  afford  the  medical  attendant  the 
opportunity  of  noting  the  first  appearance  and  gradual 
development  of  a  murmur  over  the  aorta  in  addition  to  the 
accentuated  second  sound. 

The  loudness  or  character  of  the  murmur,  or  the  extent 
to  which  it  is  conducted  along  the  aorta,  does  not  give  us 
much  help.  Hamiic  aortic  murmurs  are  usually  soft  and 
smooth,  but  so  also  may  murmurs  be  which  are  due  to 
extreme  narrowing.  It  has  been  stated  by  some  that  when 
the  margins  of  the  thickened  valves  are  smooth  and  rounded 
there  may  be  no  murmur  in  spite  of  considerable  narrow- 
ing ;  but  if  the  fact  be  true,  the  explanation  can  scarcely 
be  accepted,  since  it  is  not  the  friction  of  the  blood  against 
the  valves  as  it  passes  over  them  which  generates  sonorous 
vibrations,  but  the  eddies  produced  by  the  passage  of  the 
blood  through  a  small  orifice  into  a  large  channel.  A 
more  probable  explanation  is  weakness  of  the  ventricle  and 
languid  propulsion  of  the  blood  which  may  render  the 
murmur  weak  or  inaudible  ;  thus  the  gradual  enfeeblement 
and  ultimate  disappearance  of  a  systolic  aortic  murmur  may 
be  a  serious  prognostic  indication.  The  loudest  murmurs, 
such  as  have  already  been  mentioned,  are  most  frequently 
produced  by  rigidity  or  deformity  of  one  or  more  of  the 
cusps  or  by  a  calcareous  deposit  in  the  valve,  or  some- 
times by  a  delicate  band  stretched  across  a  part  of  the 
orifice,  but  it  would  not  be  safe  to  conclude  that  all  loud 
murmurs  are  harmless.  All  we  can  safely  infer  is  that  a 
long,  loud  murmur  indicates  a  vigorous  ventricular  systole 
which  is  a  good  prognostic  element. 

It  is  thus  evident  that  from  the  murmurs  alone  it  may 
be  impossible  to  make  a  certain  diagnosis  of  aortic  stenosis, 
and  still  less  to  estimate  the  amount  of  the  constriction. 

The  Heart :  Estimation  of  Degree  of  Stenosis  by  Degree  of 


n6  HEART  DISEASE. 

Cardiac  Hypertrophy. — We  turn,  then,  to  the  condition  of 
the  heart.  If  there  is  actual  obstruction  its  existence  will 
be  betrayed  either  by  the  changes  in  the  walls  and  cavities 
which  are  required  in  order  to  overcome  it,  or  by  some 
evidences  of  derangement  in  the  circulation. 

The  change  by  which  aortic  obstruction  will  be  over- 
come will  be  more  or  less  pure  hypertrophy  of  the  left 
ventricle.  This  does  not  bring  the  heart  to  the  gigantic 
size  which  it  reaches  as  a  consequence  of  aortic  regurgi- 
tation. The  apex  beat  will  be  lower  than  the  normal 
position  by  an  intercostal  space,  or  perhaps  more,  but  it 
will  not  be  greatly  displaced  outwards ;  it  will  be  a  well- 
defined  and  deliberate  push  of  no  great  violence.  The 
first  sound  here  will  be  dull  and  prolonged,  and  not  very 
loud  ;  perhaps  accompanied  by  a  murmur  which  may  be 
mitral,  but  most  commonly  is,  in  the  early  period  of  the 
disease,  the  aortic  murmur  conducted  to  the  apex  by  the 
walls  of  the  left  ventricle.  The  other  sounds  will  present 
nothing  remarkable,  except  that  the  aortic  second  sound 
will  be  weak.  If  we  get  such  evidence  of  hypertrophy  of 
the  left  ventricle  as  this,  i.e.  the  downward  displacement 
and  definite  push  of  the  apex  with  a  prolonged  first  sound, 
in  a  young  person  without  kidney  disease,  together  with 
a  systolic  aortic  murmur,  there  can  be  no  hesitation  in 
inferring:  stenosis  of  the  aortic  orifice.  At  and  after  middle 
age  it  would  be  necessary  to  consider  whether  the  hyper- 
trophy might  not  have  been  produced  by  long-continued, 
antecedent  resistance  in  the  peripheral  circulation  and  high 
arterial  tension ;  but  in  this  case  the  apex  would  usually  be 
less  defined,  the  first  sound  louder  and  less  deliberate,  and 
the  aortic  second  sound  much  accentuated.  When  aortic 
incompetence  has  preceded  the  stenosis,  as  is  often  the  case 
when  it  is  due  to  acute  endocarditis,  the  left  ventricle  will 
attain  a  greater  size  by  reason  of  the  previous  dilatation  to 
which  hypertrophy  has  succeeded. 


AORTIC  STENOSIS.  1*7 

The  Pulse. — Almost  more  important  than  the  hyper- 
trophy of  the  left  ventricle  will  be  the  character  of  the 
pulse.  The  orifice  being  narrowed,  the  blood  discharged 
from  the  ventricle  will  require  more  time  to  pass  through 
it,  and  the  pressure  in  the  arterial  system  will  not  at  once 
rise  to  its  maximum  ;  in  other  words,  the  so-called  percus- 
sion element  of  the  sphygmographic  trace  will  be  weakened 
and  the  pulse  wave  will  be  long  and  slow,  not  striking  the 
finger  or  lever  abruptly  and  vigorously,  but  raising  it  gradu- 
ally. The  artery  will,  for  the  most  part,  be  small  and  full 
between  the  beats  of  the  pulse.  A  large  sudden  pulse  is 
incompatible  with  aortic  stenosis  unaccompanied  by  regur- 
gitation, and  Avhen  it  is  a  question  whether  or  not  an  aortic 
systolic  murmur  is  due  to  obstruction  at  the  orifice,  the 
pulse  becomes  the  most  certain  criterion  to  which  we  can 
appeal ;  if  there  is  an  apparent  contradiction  between  the 
indications  of  the  heart  and  those  of  the  pulse,  the  latter 
must  dominate. 

For  instance,  if  with  a  systolic  and  diastolic  aortic 
murmur  and  a  hypertrophied  heart,  the  pulse  is  large, 
sudden  and  collapsing,  we  shall  infer  that  there  is  no  real 
stenosis  of  the  aortic  orifice  ;  if,  on  the  other  hand,  the 
pulse  lacks  these  features  characteristic  of  aortic  incom- 
petence, we  shall  conclude  that  there  is  aortic  stenosis 
which  has  interfered  with  their  development ;  and  we  shall 
estimate  the  degree  of  stenosis  from  the  extent  to  which  it 
has  modified  the  pulse. 

A  systolic  murmur  heard  over  the  aortic  valves  and 
along  the  aorta  will  not,  in  the  absence  of  cardiac  hyper- 
trophy and  the  long,  small  pulse  described  above,  indicate 
stenosis  of  the  aortic  orifice,  and  even  when  there  is  hyper- 
trophy, if  the  pulse  is  large,  short  and  abrupt,  there  can  be 
no  real  narrowing. 


n8  HEART  DISEASE. 

Effects  of  the  Disease  :  Symptoms. 

When  the  constriction  is  moderate  in  amount  and  is  a 
result  of  endocarditis,  in  a  young  subject  the  heart  will 
usually  undergo  hypertrophy  sufficiently  to  overcome  the  ob- 
struction, and  no  serious  or  troublesome  symptoms  will  arise. 
In  severe  cases  there  may  be  dyspnoea  and  anginoicl  pains. 
There  is  a  tendency  for  the  constriction  to  increase,  and 
when  this  is  so  considerable  as  to  have  given  rise  to  great 
hypertrophy  of  the  left  ventricle,  the  latter  is  sure  to  give 
out  sooner  or  later.  As  a  consequence  of  the  deficient  pro- 
pulsive power  resulting  therefrom,  there  will  be  a  tendency 
to  systemic  stagnation,  and  as  a  result  of  the  incomplete 
emptying  of  the  ventricular  cavity  in  systole,  there  will  be 
insufficient  room  for  the  whole  contents  of  the  left  auricle 
in  diastole,  and  consequent  back  pressure  through  the  left 
auricle  and  pulmonary  circulation.  Mitral  incompetence 
may  ensue  as  a  result  of  the  giving  out  of  the  left 
ventricle,  but  there  will  also  be  other  injurious  influences 
at  work  which  may  give  rise  to  regurgitation  in  the 
following  way :  The  pressure  in  the  ventricular  cavity 
will  be  greatly  increased  owing  to  the  powerful  contraction 
of  the  muscular  walls,  which  is  necessary  to  overcome  the 
obstruction  at  the  orifice  ;  as  a  consequence  of  this,  there  is 
a  constant  and  severe  strain  upon  the  flaps  of  the  mitral 
valve  and  the  chordse  tendinete,  so  that  eventually  they 
become  stretched  or  give  way,  and  mitral  incompetence 
results,  or  chronic  degenerative  changes  may  take  place, 
leading  to  thickening  and  contraction  of  the  valves  and 
cords.  It  will  thus  be  seen  that  in  aortic  stenosis  of  any 
severity  there  is  little  chance  of  the  mitral  valve  escaping 
damage  in  the  long  run,  and  if  it  has  at  the  outset  been 
injured  by  the  same  attack  of  endocarditis  which  gave  rise 
to  the  aortic  mischief,  the  outlook  is  far  more  serious.  The 
barrier    formed   by   the   mitral    valve    being   thus    broken 


AORTIC  STENOSIS.  "9 

down,  the  door  is  open  to  backward  pressure  through  the 
auricle,  which  will  take  effect  upon  the  pulmonary  circula- 
tion and  right  ventricle.  It  has  been  said  by  some  that 
timely  yielding  of  the  mitral  valve  acts  as  a  safety  valve, 
as  tricuspid  regurgitation  is  supposed  to  do  for  the  right 
ventricle,  preventing  sudden  death  through  over-distension 
and  consequent  paralysis  of  the  left  ventricle.  This  view 
does  not  commend  itself  to  my  judgment,  and  must,  in  the 
nature  of  things,  be  purely  hypothetical.  There  can  be  no 
doubt  that  the  establishment  of  mitral  regurgitation  marks 
a  downward  step  and  renders  the  prognosis  grave.  The 
obstacle  to  the  outflow  of  blood  from  the  ventricle,  which 
has  given  rise  to  the  whole  train  of  consequences,  remains 
irremovable,  and  the  setting  in  of  mitral  symptoms  marks 
the  failure  of  compensation. 

Prognosis. 

Nearly  all  authors  concur  in  making  aortic  stenosis  the 
least  dangerous  of  the  valvular  affections,  and  on  a  priori 
considerations  such  would  seem  to  be  probable  ;  but  this 
conclusion  will  scarcely  seem  quite  secure  if  the  cases  of 
systolic  aortic  murmur  without  actual  narrowing  of  the 
orifice  are  eliminated.  Just  as  the  inclusion  of  all  cases  in 
which  a  systolic  aortic  murmur  is  heard  makes  aortic  stenosis 
apparently  the  most  frequent  valvular  disease,  while  on 
post-mortem  evidence  it  is  seen  to  be  the  least  common,  so 
the  dilution  of  the  death-rate  by  the  cases  in  which  no 
real  narrowing  exists  makes  it  appear  to  be  the  least  fatal. 
The  relative  danger  of  real  stenosis  cannot  be  estimated 
with  confidence,  but  it  is  certainly  greater  than  has  been 
supposed,  and  though,  perhaps,  it  is  not  so  serious  as  aortic 
incompetence  or  mitral  stenosis,  it  is  more  so  than  mitral 
incompetence.  The  average  age  of  the  cases  of  this  disease 
in  the  post-mortem  statistics  referred  to  in  the  chapter  on 
prognosis  was  about  forty,  and  would  have  been  higher  had 


120  HEART  DISEASE. 

deaths  by  intercurrent  independent  disease  been  excluded. 
The  age  of  the  oldest  patient  among  these,  however,  was 
fifty-three;  this  would  bear  out  the  above  statement  that 
aortic  stenosis  must  be  looked  upon  as  more  dangerous 
than  mitral  incompetence,  of  which  numerous  examples  are 
known  to  have  reached  the  age  of  seventy. 

There  is  no  risk  of  sudden  death  as  in  aortic  incompe- 
tence, and  there  is  little  danger  as  long  as  the  patient  is  free 
from  symptoms ;  but  when  once  dropsy  has  set  in  from  back 
pressure  due  to  dilatation  of  the  left  ventricle,  there  is 
a  smaller  possibility  of  recovery  than  in  other  valvular 
affections.  For  when  the  left  ventricle  has  given  way 
under  the  resistance  it  encounters,  it  has  little  chance  of 
regaining  its  normal  condition,  since  the  resistance  persists 
undiminished,  and  there  is  no  other  compensatory  influence 
which  can  be  called  upon.  Further,  if  the  break-down 
occurs  after  middle  life,  it  is  probable  that  degenerative 
change  is  taking  place  in  the  hypertrophied  left  ventricle, 
which  will  render  the  prognosis  still  more  unfavourable. 

In  regard  to  this  it  must  be  borne  in  mind  that  at  and 
after  middle  age,  a  systolic  aortic  murmur  appearing  for  the 
first  time  may  be  indicative  of  degenerative  change,  and 
obstruction  is  the  smallest  of  the  dangers  to  which  degenera- 
tive change  in  or  about  the  root  of  the  aorta  may  give 
rise.  The  loss  of  flexibility  in  the  valve  Avhich  gives 
rise  to  obstruction  may  permit  of  regurgitation.  Again, 
the  degeneration  may  affect  one  of  the  sinuses  of  Valsalva 
and  produce  aneurysm  here,  or  may  implicate  the  orifice 
of  the  coronary  arteries,  and  by  cutting  off  the  supply  of 
blood  lead  to  fatty  change  in  the  walls  of  the  heart.  Any 
murmur  at  the  aortic  orifice,  then,  in  an  elderly  person, 
must  be  looked  upon  as  a  possible  forerunner  of  serious 
disease,  though  I.  have  known  of  cases  in  which  a  rough 
systolic  murmur  has  been  present  for  upwards  of  ten  years 
without  any  serious  symptoms  arising. 


aortic  stenosis.  121 

Treatment. 

In  regard  to  the  treatment  of  aortic  stenosis,  there  is 
little  to  add  to  what  has  been  said  on  the  treatment  of 
valvular  disease  in  general.  We  cannot  hope  to  rectify  the 
constriction  which  has  already  taken  place,  and  can  do 
little  to  modify  the  process  of  narrowing,  which  may  be 
going  on  as  a  result  of  cicatricial  contraction,  or  adhesion 
of  the  valvular  curtains,  after  acute  endocarditis  has 
subsided.  When,  however,  the  valves  are  being  damaged 
by  a  chronic  inflammatory  process  due  to  syphilis,  benefit 
may  be  sometimes  obtained  by  the  administration  of  large 
doses  of  iodide  of  potassium. 

Supposing  the  contraction  of  the  aortic  orifice  to  have 
reached  a  certain  point  and  become  stationary ;  the  dangers 
likely  to  arise  out  of  this  condition  will  be,  at  an  early 
period,  an  imperfect  degree  of  compensatory  hypertrophy 
and  later  degeneration  of  the  hypertrophied  muscular  wall, 
with,  in  both  cases,  secondary  dilatation  of  the  left  ventricle. 
From  this,  mitral  incompetence  may  result,  and  subsequently 
right  ventricle  failure  with  its  train  of  symptoms  of  venous 
obstruction. 

The  hypertrophy  is  usually  sufficient  in  the  first  instance, 
as  the  contraction  of  the  orifice  takes  place  slowly,  so  that 
the  structural  increase  can  keep  pace  with  it,  provided  that 
the  patient  is  a  young  subject.  A  moderate  degree  of 
constriction  may  therefore  exist  for  years  without  apparently 
affecting  the  health  or  well-being,  or  interfering  with 
ordinary  occupations,  giving  rise  to  no  symptoms  except 
perhaps  shortness  of  breath  and  precordial  pain  on  too 
great  exertion.  Even  considerable  stenosis  is  not  incom- 
patible with  moderate  exercise  and  work  and  apparent 
health. 

Exceptions  occur  when  the  patient  is  weak  and  anaemic, 
either  as  a  result  of  protracted  illness,  or  from  other  causes, 


122  HEART  DISEASE. 

and  nutrition  being  poor,  the  hypertrophy  is  inadequate 
and  accompanied  by  dilatation.  In  such  cases  prolonged 
rest  may  be  of  great  service. 

Secondary  dilatation  and  break-down  of  the  left  ventricle 
is  to  be  averted  by  carefully  avoiding  over-exertion,  fatigue, 
and  anxiety,  and  by  attention  to  general  health.  Modera- 
tion in  food  and  drink  is  necessary,  as  the  amount  of 
exercise  which  can  be  taken  is  limited,  and  anything  that 
may  lead  to  high  arterial  tension  and  increased  peripheral 
resistance  is  especially  to  be  guarded  against.  Tonics  may 
be  given  when  required,  and  ansernia  is  to  be  combated  by 
all  means  in  our  power.  The  protracted  administration  of 
digitalis  is  of  very  questionable  utility.  When  the  left 
ventricle  has  begun  to  give  way,  and  symptoms  of  back- 
ward pressure  through  the  lungs  and  embarrassment  of 
the  right  ventricle  supervene,  then  digitalis  and  similar 
remedies  will  be  of  service.  If,  however,  these  symptoms 
have  come  on  insidiously,  and  are  not  traceable  to  over- 
exertion, chill,  or  any  definite  cause,  drugs  will  rarely  be 
able  to  improve  materially  the  condition  of  the  patient  or 
postpone  for  long  the  fatal  termination. 

When  the  hypertrophied  walls  of  the  heart  have  begun 
to  undergo  degeneration,  and  there  is  precordial  pain  and 
oppression,  the  administration  of  nitro-glycerine  and  nitrites, 
or  the  nitrates  of  erythrol  and  mannitol,  by  diminishing  the 
arterio-capillary  resistance,  and  thus  relieving  the  stress 
on  the  left  ventricle,  will  often  afford  the  heart  distinct 
relief,  and  produce  a  general  amelioration  of  symptoms. 
These  drugs  may  be  given  at  the  same  time  with  digitalis. 

On  the  other  hand,  I  have  more  than  once  known  aconite, 
given  with  a  similar  object,  completely  overthrow  the 
compensation  established  by  hypertrophy,  and  cause  rapid 
cardiac  dilatation,  with  frequent  Aveak  and  small  pulse 
accompanied  by  pallor  and  cold  sweats. 


CHAPTER  X. 
AORTIC   INCOMPETENCE. 

etiology  —  physical  signs — the  diastolic  murmur  : 
directions  in  which  it  is  conducted— presystolic 
murmur,  its  significance — modification  of  the 
aortic  second  sound — pulsation  of  arteries — 
capillary  pulsation  —  the  collapsing  pulse  — 
pulsus  bisferiens  —  irregular  pulse— estimation 
of  the  amount  of  regurgitation  from  the 
character  of  the  murmuk,  of  the  aortic  second 
sound,  of  the  pulse,  and  the  changes  in  the 
heart  — aortic  incompetence  due  to  syphilis  and 
causes  other  than  acute  endocarditis— symptoms 
— prognosis — treatment. 

Etiology. 

The  commonest  cause  of  this  affection  in  childhood  and 
early  adult  life  is  acute  endocarditis.  As  the  clinical 
features  of  aortic  incompetence  which  develops  in  later  life 
from  other  causes,  differ  materially,  discussion  of  these 
will  be  deferred  till  later  on  in  this  chapter. 

Physical  Signs. 
The  Diastolic  Murmur. — The  diagnostic  sign  of  this  con- 
dition is  a  murmur  produced  by  the  backward  rush  of  the 
blood  from   the   aorta   into   the   left   ventricle    during   its 


124  HEART  DISEASE. 

diastole.  Two  forces  will  be  at  work  in  its  production — the 
suction  action  of  the  ventricle,  and  the  pressure  in  the 
arterial  system  generally  and  in  the  aorta  in  particular,  due 
to  the  elastic  recoil  of  the  walls  of  the  great  vessels.  The 
cause  of  the  murmur  is  not  necessarily  roughness  or  irregu- 
larity of  the  valves  or  orifice  ;  it  may  be  due  partially  or 
entirely  to  the  vibrations  generated  by  the  passage  of  liquid 
through  a  constricted  point  in  a  channel,  into  a  large  cavity 
beyond. 

The  seat  of  production  of  the  murmur  being  the  valves 
which  encircle  the  root  of  the  aorta,  the  point  on  the 
surface  of  the  chest  immediately  over  and  nearest  to  the 
origin  of  the  sound  will  be  close  to  the  left  margin  of 
the  sternum  at  the  level  of  the  third  cartilage  ;  but  it  is  not 
always  here  that  the  murmur  is  best  heard,  as  the  con  as 
arteriosus  of  the  pulmonary  artery  is  interposed  between  the 
aorta  and  the  chest  wall. 

The  murmur  is  conducted  in  various  directions,  and  the 
seat  of  its  maximum  intensity  differs  in  different  cases.  It 
is,  with  rare  excejotions,  audible  in  the  so-called  aortic  area 
just  outside  the  right  edge  of  the  sternum  in  the  second 
intercostal  space,  or  over  the  second  costal  cartilage,  and 
is  usually  conducted  upwards  from  this  point  along  the 
sternal  margin  as  far  as  the  sterno-clavicular  articulation, 
though  losing  rapidly  in  intensity  the  while.  It  can 
frequently  be  followed  downwards  along  the  side  of  the 
sternum  to  the  fourth  space,  or  even  lower,  sometimes  with 
increasing  intensity  over  one  or  two  ribs ;  it  is  also  fre- 
quently heard  along  the  sternum  itself,  or  to  the  left  of  it, 
the  seat  of  maximum  intensity  being  frequently  in  the 
fourth  or  fifth  spaces  near  the  left  edge  of  the  sternum, 
where  it  may  be  audible  when  not  heard  over  the  aortic 
area.  It  may  again  be  audible  at  the  apex  after  having 
been  lost  over  the  right  ventricle,  but  it  is  usually  weakened 
here,  and  is  not  at  its  loudest.     Another  point  at  which  it 


AORTIC  INCOMPETENCE.  125 

may  be   heard  is  the  third   left    space    exactly   over    the 
pulmonic  valves  or  artery. 

Cause  of  the  Conduction  of  the  Murmur. — In  a  certain 
degree  we   may  say  that   the  distribution  of  the  murmur 
described   is   explained   by   its   conduction   downwards   by 
the  current   of  the   regurgitant   blood,  and   this  must   be 
held  to  account  for  the  difference  between  obstructive  and 
regurgitant  aortic  murmurs,  in  regard  to  the  points  on  the 
chest  wall  where  they  are  best  heard.    But  the  direction  which 
the  blood  takes  will  be  towards  the  apex,  and  if  the  current 
carried  the  murmur,  it  would  be  at  the  apex  that  we  should 
hear  it  most  distinctly,  which  is  not  the  case.     The  truth  is 
that  we  are  apt  to  lose  sight  of  the  fact  that  much  more  blood 
enters  the  ventricle  from  the  auricle  than  from  the  aorta — 
any  other  state  of  things  would  be  incompatible  with  onward 
movement  of  the  blood  in  the  systemic  arteries,  and  therefore 
with  life — and  also  that  the  regurgitant  stream  through  the 
valves  is  comparatively  small  if  rapid.     We  are  also  perhaps 
given  to  figure  in  our  imagination,  this  stream  as  falling 
into  an  empty  vessel,  whence  has  arisen  such  an  explanation 
as  the  collision  of  the  blood  with  the  ventricular  wall,  to 
account  for  some  abnormal  sound  or  other.     The  ventricle  is 
never   an   empty  cavity  into  which    blood   can   fall   with 
violence  as  into  a  bottle    or  jar ;   there  is  no  large  and 
powerful  stream  rushing  straight  from  the  aorta  down  to  the 
apex  ;  during  diastole,  in  a  case  of  aortic  insufficiency,  there 
must  be  complicated  cross  currents  in  the  ventricle,  rendering 
conduction  of  sound  in  any  definite  direction  impossible. 
The  vibrations,  then,  must  be  conveyed  by  the  walls  of  the 
ventricles,  and  not  by  the  contained  blood,  or  at  any  rate  the 
blood  thrown  into  sonorous  eddies  will  communicate  the  vibra- 
tions to  all  parts  of  the  ventricular  wall  indifferently,  and  not 
impinge  upon  any  special  point  carrying  thither  the  sound. 
Presystolic    Murmur. —  Sometimes,    more    usually    when 
there  is  stenosis   as   well   as   incompetence   of  the   aortic 


126  HEART  DISEASE. 

orifice,  a  presystolic  murmur  is  heard  in  the  region  of  the 
apex,  resembling  very  closely  that  of  mitral  stenosis,  which 
does  not,  however,  denote  constriction  of  the  mitral  orifice. 
This  is  sometimes  termed  the  Flint  murmur,  as  it  was  first 
described  by  him.  It  is,  of  course,  possible  that  mitral 
stenosis  may  co-exist  with  double  aortic  disease ;  but  in 
some  Cases  in  which  a  presystolic  murmur  has  been  audible 
at  the  apex,  together  with  a  systolic  and  diastolic  murmur 
in  the  aortic  area,  the  mitral  orifice  has  been  found  to  be 
normal  at  the  autopsy,  and  the  only  lesion  has  been 
constriction  and  incompetence  of  the  aortic  orifice.  The 
following  explanation  of  the  origin  of  this  murmur  has 
been  suggested.  The  mitral  and  aortic  orifices  are  in 
close  apposition,  and  it  is  probable  that  the  regurgitant 
stream  from  the  aorta  impinges  to  a  certain  extent  on 
the  anterior  or  aortic  flap  of  the  mitral  valve.  It  is  con- 
ceivable that  the  murmur  may  be  due  to  this  flap  of  the 
mitral  valve  being  thrown  into  vibration  by  the  regurgi- 
tant stream  from  the  aorta,  the  vibration  being  conducted  to 
the  apex  by  the  chordse  tendinepe  and  papillary  muscles, 
or,  on  the  other  hand,  that  the  backward  rush  of  blood 
from  the  aorta  prevents  the  complete  falling  back  of  this 
flap  of  the  mitral  valve,  so  that  some  actual  obstruction  of 
the  mitral  orifice  results,  giving  rise  to  a  presystolic  murmur. 
Violent  Arterial  Pulsation. — One  of  the  most  striking 
features  in  aortic  regurgitation  is  the  sudden,  abrupt,  and 
violent  pulsation  of  the  arteries  throughout  the  body,  most 
conspicuous  in  the  carotids.  So  marked  is  this  that  one  can 
often  make  a  diagnosis  at  sight.  The  pulse  is  visible  at  the 
wrist,  the  brachials  at  the  bend  of  the  elbow  throw  them- 
selves into  violent  curves,  the  femoral  and  anterior  tibial 
arteries  are  scarcely  less  visible  ;  the  temporals,  facials,  and 
labials  may  be  seen  beating ;  even  the  digital  arteries  may 
be  seen  as  well  as  felt  to  an  unpleasant  degree.  As  was 
first  pointed  out  by  Sibson,  the  radial  pulse  is  audible  when 


AORTIC  INCOMPETENCE.  127 

the  hand  is  raised,  a  sign  more  interesting  perhaps  than 
valuable. 

The  arteries,  as  may  be  easily  seen  in  the  radial  at  the 
wrist,  are  large,  because  the  entire  contents  of  the  left 
ventricle,  expanded  to  two  or  three  times  its  normal  capacity, 
are  launched  into  the  arterial  system,  distending  it 
momentarily  to  a  corresponding  degree. 

Capillary  and  Venous  Pulsation. — Another  interesting- 
effect  is  capillary  pulsation,  a  pulsatile  reddening  of  the 
skin,  which  is  sometimes  observed  in  the  palms  of  the 
hand  when  warm,  especially  when  pyrexia  is  present,  and 
a  similar  phenomenon  may  at  any  time  be  provoked  at 
various  parts  of  the  surface,  most  conveniently  perhaps 
on  the  forehead,  by  bringing  out  a  red  patch  or  line  by 
friction,  the  margins  of  which  will  be  seen  alternately  to 
extend  and  fade,  synchronously  with  the  pulse.  This  is 
due  to  the  extension  of  the  arterial  relaxation  into  the 
capillaries,  and  when  it  is  general  the  pulsatile  movement 
of  the  blood  may  even  reach  the  veins.  To  render  this 
visible  the  hand  should  be  so  held  as  to  drop  at  the  wrist 
when  the  veins  on  the  dorsum  will  fill,  and  sometimes  will 
be  seen  to  pulsate,  not  with  the  sudden  beat  of  the  artery, 
or  like  the  rapid  flush  of  the  capillaries,  but  with  a  gentle 
and  deliberate  movement  followed  with  difficulty,  but  which 
a  filament  of  sealing-wax  across  the  vein  will  render  visible. 

Capillary  pulsation,  however,  is  not  a  phenomenon 
peculiar  to  aortic  incompetence,  as  it  may  be  produced 
sometimes  in  pneumonia,  or  phthisis,  or  enteric  fever,  or 
other  conditions  associated  with  a  pulse  of  low  tension. 

The  Pulse. — This  is  the  well-known  collapsing  or  water- 
hammer  pulse,  sometimes  named  after  Corrigan,  who  is 
believed  to  have  first  called  attention  to  it.  The  artery  at 
the  wrist  is  large.  In  the  intervals  between  the  pulsations 
it  is  empty  and  allows  itself  to  be  completely  flattened 
against  the  bone;    then  the   wave    comes  with   a   sudden 


128  HEART  DISEASE. 

violent  rush,  filling  the  vessel  and  lifting  the  fingers 
forcibly.  It  is  as  short  as  it  is  sudden,  and  the  artery  at 
once  collapses  again  under  the  pressure  of  the  fingers.  In 
order  that  all  these  features  may  be  fully  realized,  the  hand 
must  be  above  the  level  of  the  heart  and  above  the  shoulder 
or  elbow.  When  the  patient  is  lying  in  bed,  the  act  of 
giving  the  hand  for  the  pulse  to  be  felt  brings  about  this 
condition,  but  when  he  is  sitting,  as  during  an  interview  in 
the  consulting-room,  or  standing  with  the  arm  hanging 
down,  although  the  artery  may  be  large  and  the  beat 
sudden,  the  collapse  will  not  take  place. 

The  cause  of  the  collapse  is,  that  in  consequence  of  the 
loss  of  the  support  of  the  aortic  valves,  the  column  of  blood 
is  not  sustained,  and  therefore  drops  out  of  any  vessel 
which  is  above  the  level  of  the  heart  in  obedience  to 
gravity.  If,  then,  the  hand  is  hanging  down,  the  radial 
artery  remains  full,  having  above  it  a  column  of  blood  up 
to  the  arch  of  the  sub-clavian. 

The  collapsing  character  of  the  pulse  is  indispensable  as 
an  evidence  of  aortic  regurgitation,  though  certain  compli- 
cations, which  will  be  enumerated  later,  may  interfere  with 
the  degree  of  collapse. 

In  cases  of  pulmonic  regurgitation,  which  are  rarely 
met  with,  the  absence  of  the  collapsing  pulse  and  of  undue 
carotid  pulsation  will  be  the  most  important  distinguishing 
features.  Similarly  their  presence,  in  cases  where  the 
diastolic  murmur  is  heard  loudest  or  exclusively  over  the 
pulmonic  area,  will  clear  up  all  doubts  as  to  diagnosis. 

The  evidence  afforded  by  the  collapsing  pulse  is  corro- 
borated by  conspicuous  pulsation  in  the  carotid  arteries. 
This  is  visible  not  only  at  the  root  of  the  neck,  where 
pulsation  is  often  seen,  but  can  be  followed  upwards  along 
the  entire  course  of  the  artery  in  front  of  the  sterno-mastoid 
and  between  this  muscle  and  the  ramus  of  the  jaw,  also 
in  front  of  the  ear. 


AORTIC  INCOMPETENCE.  129 

The  Delay  of  Pulse. — The  pulse  in  aortic  regurgitation  is 
always  retarded  or  delayed — that  is,  there  is  an  appreciably 
longer  interval  than  normal  between  the  beat  of  the  heart 
and  the  pulsation  in  the  radial  artery,  which  varies 
according  to  the  extent  of  the  incompetence.  This  delay 
is  due  partly  to  the  collapsed  and  empty  state  of  the 
arteries  between  the  beats,  and  partly  to  their  large  size 
and  loss  of  tone.  The  tension  in  the  arterial  system  has 
to  be  considerably  augmented  by  the  launching  of  a 
large  volume  of  blood  into  the  aorta,  before  the  vessels 
are  rendered  sufficiently  tense  for  a  pulse-wave  to  be 
transmitted.  Clifford  Allbutt,*  in  his  article  on  Aortic 
Kegurgitation,  states  that  delay  of  the  pulse  seems  to  him 
to  be  "contrary  to  observation  both  physiological  and 
pathological."  He  qualifies  this  statement  later  on  in 
a  postscript,!  and  admits  that  there  is  delay,  as  shown 
by  tracings  taken  by  Dr.  Chapman  of  Hereford,  the  delay 
being  attributed  to  prolongation  of  the  cardiac  systole. 
Mackenzie  %  published  a  series  of  tracings  which  he  claims 
prove  the  opposite  of  this,  namely,  that  there  is  no  delay. 
The  explanation  of  this  conflict  of  evidence  may  be  that 
the  cases  investigated  were  of  different  types.  Mackenzie 
states  that  some  of  his  were  taken  from  cases  of  incompetence 
due  to  degenerative  changes,  and  in  these  conditions  one 
would  not  expect  much  delay,  as  the  aorta  is  converted  into 
a  rigid  inelastic  tube,  and  the  loss  of  elasticity  would  tend 
to  lessen  the  amount  of  regurgitation  and  to  do  away  with 
the  delay  which  the  expansion  of  the  walls  of  the  great 
vessels  entails.  Moreover,  in  seeking  the  clinical  evidence 
of  delay  in  the  pulse,  the  hand  is  raised  so  as  to  bring  out 
the  significant  effects  in  the  circulation,  whereas  in  instru- 
mental estimation  of  the  retardation  of  the  pulse  wave,  the 
forearm  rests  on  a  table  below  the  level  of  the  shoulder, 

*  "  System  of  Medicine,"  vol.  v.  p.  939.  f  Ibid.,  p.  965, 

%  Edinburgh  Medical  Journal,  189S. 

K 


*30  HEART  DISEASE. 

so  that  the  column  of  blood  in  the  arm  does  not  fall  back 
towards  the  heart,  tending  to  empty  the  vessel,  but  is  ready 
to  transmit  the  systolic  pressure. 

The  pulsus  bisferiens  is  sometimes  met  with  in  aortic 
incompetence,  more  commonly  when  there  is  concomitant 
stenosis.  It  is  a  peculiar  double  beat,  best  felt  when  the 
fingers  exert  a  moderate  pressure  on  the  artery,  less  than  is 
necessary  to  bring  out  fully  the  collapsing  character  of  the 
pulse,  but  more  than  is  employed  to  appreciate  dichrotism. 
It  can  be  readily  demonstrated  by  the  sphygmograph.  It  is 
produced  by  a  double  systolic  effort,  which  can  sometimes 
be  felt  or  heard  in  the  heart  itself,  and  which  frequently 
gives  rise  to  a  double  rush  of  blood  audible  in  the  carotids. 


FIG.  15. — PULSUS   BISFERIENS. 

According  to  D'Espine,  of  Geneva,  the  normal  systole  of  the 
heart  is  a  deux  temps,  or  a  double  contraction,  of  which  this  is 
an  exaggeration.  The  pulsus  bisferiens  can  not  uncommonly 
be  induced  by  an  effort,  which  throws  additional  work  on 
the  heart ;  for  instance,  in  one  case  it  was  not  present  while 
the  patient  lay  quietly  in  bed,  but  was  brought  out  when 
he  held  up  both  his  hands. 

Irregularity  of  Pulse. — Though  the  pulse  of  aortic  in- 
competence is  for  the  most  part  regular  in  force  and 
frequency,  in  advanced  cases,  especially  when  the  heart  is 
beginning  to  fail,  irregularity  of  pulse  is  not  uncommon. 
The  irregularity,  which  may  be  described  as  faltering,  is 
first  manifested  by  the  occurrence  of  a  short  and  rapid 
pulsation  of  less  force  and  amplitude  than   the   ordinary 


AORTIC  INCOMPETENCE. 


131 


wave,  and  occurring  at  irregular  intervals.  It  succeeds 
the  previous  beat  very  quickly,  and  is  followed  by  a  longer 
interval  than  usual.  It  would  seem  to  indicate  an  effort 
of  the  heart  to  supplement  an  inadequate  and  inefficient 
preceding  contraction,  or  to  be  an  abortive  systole.  Later 
on,  the  irregularity,  both  in  force  and  frequency,  becomes 
more  general  and  more  marked,  though  the  pulse  is  still 
recognizable  as  that  of  aortic  regurgitation. 

Estimation  of  the  Extent  of  the  Lesion. 

The  amount  of  blood  which  returns  into  the  ventricle 
is  a  matter  of  the  first  importance  in  estimating  the 
prospects  of  life  and  comfort  before  the  patient,  and  we 
have  now  to  consider  the  different  sources  of  information 
on  this  point. 

The  diastolic  murmur  itself  affords  but  vague  indications. 
As  has  been  already  mentioned,  it  may  be  loud  or  feeble, 
rough  or  smooth,  long  or  short.  It  usually  begins  with  an 
accent.  Speaking  generally,  a  long  loud  murmur  shows 
that  a  considerable  degree  of  pressure  is  kept  up  in  the 
aorta,  which  is  a  desirable  thing  in  itself,  and  a  proof  that 
the  heart  is  acting  with  vigour,  and  also  that  the  leakage 
of  the  valves  is  not  excessive ;  it  is  usually,  therefore,  among 
the  favourable  auguries.  On  the  other  hand,  a  weak  short 
murmur  indicating  an  opposite  state  of  things  may  be  a 
note  of  impending  danger  or  death.  But  there  are  so  many 
exceptions  to  the  rule  hinted  at  that  it  is  not  to  be  relied 
upon. 

Aortic  Second  Sound. — A  very  important  auscultatory 
sign,  however,  is  the  presence  or  absence  of  the  aortic 
second  sound.  We  must  listen  for  this,  not  at  the  apex  or 
in  the  aortic  area,  but  in  the  neck.  A  second  sound  of 
some  kind,  probably  the  pulmonic  conducted,  is  often  heard 
cat  the  apex  or  base,  but  it  has  not  the  same  favourable 


132  HEART  DISEASE. 

significance.  The  point  of  the  sign  is  this :  the  aortic 
second  sound  is  produced  by  the  sudden  tension  of  the 
aorta  and  its  semilunar  valves  at  the  moment  of  closure  of 
the  valves ;  it  is  not  their  clicking  as  they  meet,  or  the 
tension  of  the  valves  alone  under  the  column  of  blood, 
but  the  vibration  or  sudden  strain  on  the  entire  ascending 
aorta.  If,  then,  the  incompetence  is  considerable,  there 
cannot  be  the  sudden  check  to  the  column  of  blood  which 
sets  the  aorta  vibrating,  and  the  diastolic  murmur  takes 
the  place  of  the  second  sound ;  if,  on  the  contrary,  the 
leakage  is  only  small,  the  required  check  or  shock  is  given 
by  the  closing  valves,  and  the  second  sound  is  distinct, 
although  there  may  be  a  murmur.  It  is  not  the  murmur, 
which  may  be  loud  or  feeble,  that  drowns  the  second  sound 
and  prevents  it  being  heard.  In  listening  in  the  neck  over 
the  carotid  artery,  we  have  the  advantage  of  being  out  of 
reach  both  of  the  diastolic  murmur  and  of  the  pulmonic 
second  sound,  and  the  tension  in  the  aorta  must  be  real  in 
order  that  the  second  sound  may  be  heard  here.  A  second 
sound,  therefore,  heard  in  the  neck  indicates  that  the 
regurgitation  is  small  in  amount  and  is  consequently  a 
favourable  prognostic  element.  The  second  sound  is  usually 
loud  and  ringing  when  the  incompetence  is  the  result  of 
dilatation  of  the  aorta  involving  the  orifice,  but  this  is  not 
of  favourable  prognostic  significance,  as  the  lesion  is  due  to 
degeneritive  change  and  is  likely  to  be  progressive. 

The  Pulse. — The  degree  of  collapse  in  the  pulse  is  an 
important  factor  in  the  estimation  of  the  amount  of  the 
regurgitation.  The  greater  the  regurgitation,  the  more 
pronounced  will  be  the  collapsing  character  of  the  pulse. 
In  the  absence  of  any  marked  collapse  in  the  pulse,  a 
diastolic  murmur,  whatever  its  character,  would  not  indicate 
any  serious  degree  of  incompetence.  While  this  may  be 
taken  as  a  general  rule,  three  important  exceptions  must 
be  mentioned : 


AORTIC  INCOMPETENCE. 


133 


1.  Concomitant  aortic  stenosis  may  interfere  with  the 
suddenness  and  completeness  of  the  collapse,  when  the 
amount  of  regurgitation  would  have  to  be  estimated  by 
other  means  than  by  the  pulse. 

2.  In  the  last  stages  of  aortic  regurgitation,  when  the 
heart  is  failing,  there  may  not  be  sufficient  force  in  the 
cardiac  systole  to  produce  the  collapsing  pulse. 

3.  In  aortic  disease,  acquired  in  later  life  from  dilatation 
of  the  aorta  or   degenerative  changes  in  the  valves,  the 


FIG.    1G. — COLLAPSING   PULSE   OF   AORTIC    FvEGURGITATION   DUE   TO   ACUTE    ENDOCARDITIS. 


FIG.  17. 


FIGS.   18. — LOSS  OF   COLLAPSE   IN  PULSE   OF   AORTIC   REGURGITATION 
DUE   TO   DEGENERATIVE    CHANGES. 

pulse  has  not  the  typical  sudden  and  collapsing  character. 
(Figs.  17  and  18.)  This  absence  of  collapse  in  the  pulse  is 
partly  due  to  the  rigidity  and  loss  of  elasticity  in  the 
vessels,  partly  to  the  fact  that  the  incompetence  is  not  great, 
as  in  such  cases  life  is  rarely  prolonged  if  the  regurgitation 
becomes  considerable. 

The  difference  between  the  pulse  of  aortic  incompetence, 
due  to  degenerative  changes  in  the  valves,  and  the  ordinary 
collapsing  pulse  is  well  brought  out  by  a  sphygmographic 
tracing. 


134  HEART  DISEASE. 

The  Heart. — Other  evidence  as  to  the  amount  of  regurgi- 
tation is  obtained  from  the  changes  which  it  has  induced  in 
the  heart.  It  has  already  been  pointed  out  that  if  the 
normal  amount  of  blood  is  to  be  propelled  through  the 
systemic  arteries,  while  a  certain  proportion  of  that  sent 
by  each  systole  into  the  aorta  is  returned  into  the  ventricle, 
an  increase  in  the  capacity  of  the  ventricle  is  necessary. 
In  other  words,  it  must  be  dilated.  We  are  not  arguing 
that,  because  the  necessity  exists,  therefore  the  provision 
is  made,  but  showing  that  the  dilatation  always  found  is 
not  injurious  but  useful,  inasmuch  as  increased  force  in  the 
ventricular  contraction  would  not  alone  meet  the  difficulty. 

The  process  by  which  the  dilatation  is  effected  is  the 
distending  influence  of  the  backward  pressure  from  the  aorta, 
during  the  diastole  of  the  ventricle,  when  the  muscular 
fibres  are  relaxed  and  unresisting.  Finally,  hypertrophy 
results  from  the  excessive  functional  activity  imposed  upon 
the  walls  of  the  ventricle  by  the  mechanical  conditions 
present.  It  is  in  aortic  incompetence  that  the  extremes 
of  dilatation  and  hypertrophy  of  the  left  ventricle  are  met 
with,  and  we  have  the  apex  beat  displaced  downwards  to 
the  sixth,  seventh,  or  eighth  space,  and  carried  beyond  the 
nipple  or,  in  exceptional  cases,  up  to  or  beyond  the  anterior 
axillary  line.  The  apex  beat  may  be  well  defined,  or 
spread  over  a  large  area,  and  will  be  powerful.  Sometimes 
the  wall  of  the  chest  between  the  apex  and  the  sternum 
is  visibly  lifted  by  the  forcible  contraction  of  the  left 
ventricle.  Very  frequently  two  or  three  spaces,  between 
the  nipple  line  and  the  sternum,  will  be  depressed  with 
the  systole,  and  this  systolic  recession  of  intercostal  spaces 
has  been  supposed  to  prove  the  existence  of  adhesion 
between  the  pericardium  and  heart.  It  is,  however, 
frequently  only  the  result  of  atmospheric  pressure  con- 
tributing to  fill  up  the  space  left  by  the  great  diminution 
of  volume  of  the  heart  during  systole. 


AORTIC  INCOMPETENCE.  i?>i 

Estimation  of  the  Extent  of  the  Lesion  by  Degree 
of  Dilatation  and  Hypertkophy  of  the  Heart. 

The  dilatation  and  hypertrophy  being  the  effects,  are 
also,  with  certain  qualifications,  the  measure  of  the 
regurgitation,  in  the  absence  of  symptoms  such  as  con- 
spicuous breathlessness  on  very  slight  exertion,  or  faltering 
action  of  the  heart  and  tendency  to  fainting  or  giddiness. 
The  most  important  qualification  is  that  arising  out  of 
the  inability  of  the  heart  to  take  on  these  compensatory 
changes  late  in  life ;  so  that  when  aortic  insufficiency 
develops  for  the  first  time  after  the  age  of  thirty,  an 
opinion  as  to  its  degree,  and  as  to  the  danger  attending  it, 
can  only  be  arrived  at  after  prolonged  observation  and 
repeated  examination.  It  is  an  interesting  and  important 
question  up  to  what  age  effectual  compensation  for  serious 
aortic  regurgitation  is  possible.  In  my  own  experience  all 
really  satisfactory  examples  have  been  among  those  in 
whom  the  valvular  lesion  has  been  established  under  the 
age  of  twenty.  Cases  have  come  under  my  observation  in 
hospital  practice  in  which  the  valves  have  been  extensively 
damaged  between  the  age  of  twenty  and  thirty,  and  the 
patients  have  remained  under  observation  for  some  time 
afterwards,  without  developing  symptoms  of  cardiac  failure  ; 
but  such  cases  are  too  soon  lost  sight  of  for  trustworthy 
conclusions  to  be  based  upon  them. 

The  amount  of  dilatation  attending  a  given  degree  of 
incompetence  will  also  vary  according  to  the  amount  and 
duration  of  the  care  bestowed  upon  the  patient  during  the 
first  few  months  of  its  existence.  If  he  has  been  allowed  to 
leave  his  bed  too  early  and  engage  in  exercise,  or  has 
undertaken  work  before  the  heart  has  fully  recovered  from 
the  effects  of  acute  disease,  the  dilatation  will  have  gone 
further  than  would  have  been  the  case  if  due  precautions 
had  been   observed   till   the   strength   was   fully   restored. 


136  HEART  DISEASE. 

Dilatation,  moreover,  may  be  increased  during  subsequent 
illness  attended  with  pyrexia  or  ansemia.  In  all  such  cases, 
however,  if  the  extent  of  the  changes  in  the  cavities  and 
walls  of  the  heart  does  not  accurately  correspond  with  the 
degree  of  change  in  the  valves,  it  indicates  the  extent  to 
which  the  functional  efficiency  of  the  heart  is  endangered. 

Aoetic  Incompetence  due  to  other  Causes  than 
Acute  Endocarditis. 

In  the  account  just  given  of  the  physical  signs  of  aortic 
incompetence,  reference  has  been  made  from  time  to  time 
to  differences  observed  when  the  valvular  disease  is 
established  during  or  after  middle  life,  and  from  causes 
other  than  rheumatism.  Such  causes  are  syphilitic  affection 
of  the  valves  and  the  wall  of  the  aorta,  degenerative 
changes  included  under  the  general  term  atheroma,  and 
rupture  of  a  cusp  of  the  valve. 

Syphilis  may  be  suspected  as  the  cause  of  aortic 
incompetence,  which  comes  on  in  early  adult  life  or  middle 
age,  and  is  not  traceable  to  rheumatic  endocarditis  or  to 
gout  or  high  arterial  tension.  It  is  usually  associated  with 
degenerative  changes  and  dilatation  of  the  aorta.  Aneurysm 
is  indeed  more  common  than  aortic  incompetence  as  a 
result  of  syphilis.  The  regurgitation  may  rapidly  become 
considerable,  and  as  regards  the  murmur  and  the  character 
of  the  pulse,  there  will  be  no  important  deviations  from 
the  description  given.  The  principal  difference  will  arise 
from  the  fact  that  the  heart-walls  and  cavities  do  not  so 
readily  take  on  compensatory  changes;  consequently  the 
relation  between  the  degree  of  dilatation  and  hypertrophy 
which  makes  the  latter  approximately  a  criterion  by  which 
to  estimate  the  former,  no  longer  holds  good.  There  may, 
therefore,  be  considerable  regurgitation  with  comparatively 
little  enlargement  of  the  heart. 


AORTIC  INCOMPETENCE.  137 

Atheroma  of  the  Aorta. — Atheroma  may  involve  the 
aortic  valves  or  give  rise  to  dilatation  of  the  aorta,  in- 
cluding the  aortic  orifice,  and  thus  produce  insufficiency. 
When  the  incompetence  is  the  result  of  such  degenerative 
changes,  there  will  be  hypertrophy  and  dilatation  of  the 
heart,  not,  however,  induced  by  and  compensatory  of 
the  valvular  defect,  but  developed  antecedently  to  it  by 
the  high  arterial  tension  which  has  given  rise  to  the 
aortic  disease.  The  pulse  will  exhibit  only  partially  and 
imperfectly  the  collapsing  character ;  the  artery  will  be 
large,  and  the  wave  sudden  and  brief;  but  when  the  hand 
is  held  up  the  vessel  does  not  collapse,  but  can  be  rolled 
under  the  finger  throughout  the  diastolic  interval.  It  will 
be  visible,  not  however  from  the  sudden  filling  of  the 
previously  collapsed  artery,  but  from  the  artery  being 
thrown  into  curves.  Further,  there  will  not  be  the  marked 
loss  of  time  between  the  apex  beat  and  the  pulse  at  the 
wrist.  The  second  sound  is  usually  heard  in  the  neck, 
and  has  the  low  pitch  and  ringing  character  indicative  of 
dilatation  of  the  aorta  and  high  arterial  tension.  Very 
frequently  the  diastolic  murmur  is  audible  across  the 
manubrium,  along  the  course  of  the  aorta. 

The  insufficiency  in  such  cases  is  produced,  not  simply 
by  changes  in  the  valve,  but  by  concurrent  dilatation  of  the 
aorta  implicating  its  orifice,  which  is  sometimes,  indeed,  so 
stretched  that  the  valves,  even  when  retaining  their  normal 
size,  fail  to  close  it,  and  the  actual  amount  of  regurgitation  can 
never  become  considerable  without  producing  fatal  syncope. 

Rupture  of  Valve. — Rupture  of  a  valve  is  always  a 
very  serious  lesion.  It  may  occur  as  the  result  of  severe 
exertion  when  the  valve  has  been  weakened  by  degenerative 
changes.  The  valve  affected  is  usually  the  aortic,  and  the 
sudden  and  severe  strain  on  the  heart,  which  has  no  time 
to  accommodate  itself  to  the  altered  conditions  of  the  circu- 
lation, leads  to  dilatation   of  the    left    ventricle   and  the 


138  HEART  DISEASE. 

consequent  onset  of  severe  symptoms  wnen  the  rupture  of  a 
cusp  is  complete.  The  patient  may  be  seized  by  a  syncopal 
attack,  which  will  at  once  prove  fatal.  He  may,  however, 
appear  to  progress  favourably  for  some  time,  but  will  rarely 
recover  sufficiently  to  be  able  to  go  about  again  as  usual, 
for  the  accident  usually  takes  place  at  a  time  in  life  when 
degenerative  changes  are  already  beginning  to  take  place 
in  the  walls  of  the  heart,  and  it  is  incapable  of  under- 
going sufficient  hypertrophy  to  compensate  for  the  valvular 
lesion.  Hence  the  ultimate  cause  of  death,  if  the  patient 
survives,  is  a  gradual  stasis  of  the  circulation,  the  pre- 
monitory indications  being  a  rapid  increase  in  the  size  of 
the  liver,  with  dilatation  of  the  right  ventricle  following  on 
that  of  the  left,  and  later  the  onset  of  cedema  of  the  ex- 
tremities. It  may  be  some  weeks  or  months  after  the 
accident  before  the  fatal  termination  ensues. 

The  early  symptoms,  however,  are  not  necessarily  so 
severe. 

In  a  case  that  was  under  my  care  at  St.  Mary's  Hospital 
in  1893,  the  patient,  a  man  aged  fifty-two,  walked  up  to  the 
casualty  room,  complaining  that  he  could  not  use  his  right 
arm,  and  saying  that  he  thought  he  had  sprained  it  while 
lifting  a  heavy  weight.  The  history  of  the  accident  was 
that  he  was  carrying  a  heavy  bag  on  his  shoulder ;  and 
when  throwing  it  off  his  shoulder  he  tried  to  prevent 
it  falling  with  too  much  violence  on  to  the  ground  by 
catching  hold  of  it  with  his  right  hand.  He  then  felt  a 
sudden  pain  in  his  arm  and  chest,  and  was  violently  sick. 
He  walked  up  to  the  hospital,  apparently  without  much 
discomfort.  He  was  somewhat  pale,  but  was  not  suffering 
from  dyspnoea,  and  complained  chiefly  of  his  right  arm. 
On  examination,  the  right  radial  pulse  was  found  to  be 
absent  owing  to  thrombosis  of  the  brachial  and  axillary 
arteries.  The  pulse  in  the  left  radial  was  98,  regular  in 
force  and  frequency,  slightly  collapsing  ;  respirations,  18. 


AORTIC  INCOMPETENCE.  139 

On  examining  the  heart,  the  apex  beat  was  found  to  be 
in  the  fifth  space,  just  inside  the  nipple  line ;  a  faint  systolic 
and  diastolic  murmur  were  audible  at  the  apex,  and  a 
diastolic  murmur  was  also  heard  at  the  aortic  cartilage  and 
down  the  sternum.     The  liver  was  not  enlarged. 

He  remained  in  hospital  from  April  22  till  May  13, 
when  he  left  at  his  own  request.  During  this  time  no 
serious  symptoms  had  developed,  and  he  had  been  up  and 
walking  about  the  ward  without  any  discomfort  beyond  a 
little  shortness  of  breath. 

Bather  more  than  a  fortnight  later,  on  May  30,  he 
came  back  to  the  hospital  complaining  of  extreme  short- 
ness of  breath  and  swelling  of  the  legs.  The  pulse  was 
then  116,  the  respirations  34.  The  legs  were  cedematous, 
and  the  face  was  very  pale  and  ansemic.  On  examining  the 
heart,  it  was  found  to  be  much  dilated,  the  area  of  cardiac 
dulness  extending  up  to  the  third  rib  above  and  inwards  to 
the  middle  of  the  sternum,  outwards  for  half  an  inch 
outside  the  nipple  line. 

The  apex  beat  was  not  visible  or  palpable,  but  the 
sounds  were  best  heard  in  the  seventh  space,  half  an  inch 
outside  the  nipple  line.  A  systolic  and  long  soft  diastolic 
murmur  were  audible  at  that  point,  and  the  diastolic  murmur 
was  heard  down  the  sternum.  The  aortic  second  sound  was 
almost  entirely  replaced  by  the  murmur,  and  the  first  sound 
was  very  feeble.  The  liver  was  much  enlarged,  extending 
down  to  within  two  inches  of  the  umbilicus,  and  was 
pulsating. 

Kest  and  treatment  failed  to  improve  his  condition, 
which  got  steadily  worse,  the  symptoms  increasing  in 
severity  till  he  died  on  August  9,  some  ten  weeks  later. 
At  the  autopsy  it  was  found  that  the  anterior  flap  of  the 
aortic  valve  was  ruptured,  and  that  there  was  extensive 
incompetence.  There  was  considerable  dilatation  of  the 
cardiac  cavities,  and  little  or  no  compensatory  hypertrophy. 


HO  HEART  DISEASE. 


Symptoms. 


The  symptoms  in  well-marked  aortic  regurgitation  are 
those  of  deficient  and  unsustained  blood  supply  in  the 
systemic  circulation.  The  patient  is  pale,  anaemic,  short  of 
breath  on  slight  exertion,  and  liable  to  fainting  or  syncopal 
attacks,  one  of  which  may  prove  fatal.  Pain,  or  a  sense  of 
oppression  in  the  cardiac  region,  may  be  present,  amounting 
in  severe  cases  to  angina  pectoris.  There  may  be  sleepless- 
ness or  paroxysms  of  severe  dyspnoea,  and  vomiting  is 
sometimes  persistent  in  severe  cases  where  compensation 
has  not  been  established  or  suddenly  breaks  down. 

The  above  may  be  termed  "  aortic "  symptoms,  as  dis- 
tinguished from  the  train  of  symptoms  which  set  in  when 
the  mitral  valve  has  given  way  under  the  strain  and  mitral 
incompetence  is  established.  The  burden  of  compensation 
then,  as  in  mitral  disease,  falls  on  the  right  ventricle,  and 
we  get  a  train  of  "  mitral "  symptoms  in  addition  to  the 
already  existing  "  aortic  "  symptoms. 

There  will  be  back  pressure  in  the  pulmonary  veins 
with  congestion  of  the  lungs,  increased  dyspnoea,  and 
perhaps  cyanosis.  Dilatation  of  the  right  ventricle  eventu- 
ally occurs,  and  enlargement  of  the  liver  and  dropsy 
supervene. 

Secondary  mitral  symptoms  are  less  common  in  aortic 
regurgitation  than  stenosis,  as  if  the  lesion  is  severe  the 
patient  is  liable  to  sudden  death  from  syncopal  attack. 
When  stenosis  supervenes  in  a  severe  case  of  regurgitation, 
it  appears  to  have  a  beneficial  effect,  and  limits  the  amount 
of  reflux,  so  that  the  patient  has  a  better  chance  of  sur- 
viving for  a  time ;  and  it  is  in  cases  of  double  aortic  lesions 
that  we  usually  meet  with  the  train  of  secondary  mitral 
symptoms,  when  the  patient  eventually  succumbs  from 
right  ventricle  failure. 


aortic  incompetence.  141 

Pkognosis. 

When,  with  a  diastolic  murmur,  the  aortic  second 
sound  is  distinctly  audible  in  the  neck,  the  pulse  exhibits 
the  collapsing  character  only  in  a  moderate  degree,  and 
the  dilatation  and  hypertrophy  of  the  heart  are  inconsider- 
able; that  is,  when  the  physical  signs  indicate  that  the 
lesion  is  slight  in  extent,  the  patient  may  enjoy  life  and 
do  hard  work  untroubled  by  symptoms  for  many  years, 
provided  that  the  lesion  is  due  to  acute  endocarditis  and 
not  to  degenerative  changes. 

This   may  be  illustrated  by  an   example.      A  medical 
man,  aged    forty,  called   on    me   in  October,   1883,  whom 
I   had   known   and    examined   sixteen   or    eighteen    years 
previously,  when   he  was   under    Dr.    Sibson's    care   as   a 
student  at  the  hospital.     He  had  had  aortic  incompetence 
ever  since   an  attack  of  acute  rheumatism  at  the  age  of 
fourteen,  so  that  its  duration  was   twer>ty-six  years.     The 
following  is  an  account  of    the  physical  signs,  they  were 
identical  with  those  present  when  he  was  at  the  hospital : 
"  Apex  beat  in  sixth  space  not  much  below  and  very  little  to 
the  left  of  the  normal  situation,  being  a  good  push,  but  not 
violent    or    extensive ;    the   first  sound  good,   the   second 
sound    also   distinct.      A   systolic  murmur,  probably   con- 
ducted from  the  aorta,  is  audible  at  the  apex.     At  the  right 
second  intercostal  space  a  weak  systolic  murmur  is  audible, 
and  along  the  right  edge  of  the  sternum,  from  the  third 
cartilage  downwards,  over  the  lower  part  of  the  sternum  and 
over  the  left  costal  cartilages,  a  very  distinct,  long,  smooth 
diastolic  murmur  is  heard.     There  is  a  good  second  sound, 
audible  at  the   right  second   space    and   sterno-clavicular 
articulation  and  in  the  neck.     The  pulse  is  short   and  is 
felt  in  the  fingers  as  well  as   at  the  wrist,  but  is  scarcely 
collapsing ;  the  carotid  pulsation  is  marked,  but  the  pulse 
at  the  wrist  and  in  the  temporals  is  not  visible."     He  had 


142  HEART  DISEASE. 

gone  through  his  medical  studies  with  distinction,  and 
had  ever  since  carried  on  a  hard-working  country  practice, 
with  all  its  incidents  of  night-work  and  exposure  and 
excessive  fatigue.  He  could  walk  uphill  or  run  upstairs 
without  experiencing  any  inconvenience,  and  it  was  not  for 
any  cardiac  symptoms  that  he  consulted  me  in  1883. 

Aortic  incompetence  sufficient  to  abolish  the  second 
sound  in  the  neck,  and  to  give  rise  to  considerable  dilatation 
and  hypertrophy  and  to  well-marked  collapsing  pulse  is 
serious,  though  it  may  for  many  years  be  compatible  with 
apparent  health  and  strength.  The  patient  will  be  capable 
of  ordinary  work  and  exercise,  but  will  be  sooner  out  of 
breath  on  going  uphill  or  from  any  unusual  exertion  than 
a  man  in  health,  or  may  feel  suddenly  faint  and  giddy 
instead  of  losing  his  breath ;  emotion  again  will  more 
readily  induce  palpitation.  The  future  in  such  circum- 
stances must  be  estimated  on  the  principles  laid  down  in 
the  chapter  on  general  prognosis.  After  calculation  of 
the  degree  of  valvular  inefficiency,  we  must  consider  the 
tenacity  of  the  family  constitution  and  the  vigour  of  the 
individual,  as  well  as  his  age,  habits,  occupation,  and 
circumstances,  bearing  in  mind  always  that  even  in  the 
most  favourable  cases  the  nutrition  of  the  enlarged  heart 
will  not  be  well  maintained  after  middle  age,  and  that  as 
years  go  on  there  is  a  tendency  to  increased  resistance  in 
the  peripheral  circulation.  We  must  look,  therefore,  for 
failure  of  the  heart  and  accession  of  symptoms  sooner  or 
later,  at  best  long  before  the  natural  term  of  life.  There  is 
also  the  possibility  that  the  compensatory  equilibrium  may 
at  any  time  be  dangerously  disturbed  or  finally  overthrown 
by  imprudent  exertion  or  anxiety  or  acute  illness  of  any 
kind. 

The  Age  of  the  patient  at  the  time  when  the  lesion  is 
acquired  is  a  most  important  consideration  in  prognosis, 
and  a  case  may  be  quoted  to  show  how  long  a  severe  lesion 


AORTIC  INCOMPETENCE.  143 

may  be  survived  even  under  unfavourable  circumstances, 
when  the  patient  is  young,  and  the  heart  can  take  on 
compensatory  changes.  The  patient,  a  boy  of  fifteen,  came 
under  my  observation  in  1868,  when  he  was  admitted  to 
St.  Mary's  Hospital,  complaining  of  shortness  of  breath. 
His  condition  on  admission  was  as  follows  :  "  Heart  impulse 
extensive  and  violent,  apex  beat  in  the  fifth  and  sixth 
spaces  just  outside  the  nipple  line.  Loud  systolic  and 
diastolic  murmurs,  audible  over  all  the  cardiac  area, 
especially  at  the  lower  end  and  down  the  right  border  of 
the  sternum.  Pulse  large,  sudden,  and  collapsing ;  no 
second  sound  audible  in  the  neck."  The  patient  was  a 
greengrocer,  and  continued  to  do  his  work,  but  frequently 
attended  the  hospital  as  an  out-patient.  Five  years  later, 
a  mitral  systolic  murmur  first  developed,  and  by  that  time 
the  heart  was  of  great  size ;  the  apex  beat  was  in  the 
seventh  space  in  the  axillary  line,  and  was  a  forcible  thrust, 
which  could  be  seen  through  his  clothes.  Dilatation  and 
elongation  of  the  aorta  had  carried  the  outer  side  of  the 
ascending  arch  beyond  the  right  edge  of  the  sternum,  so 
that,  pressed  into  the  second,  third,  and  fourth  spaces,  the 
fingers  came  upon  marked  pulsation  and  thrill.  He  was 
still  able  to  do  his  work,  and  a  year  later,  at  the  age  of 
twenty-one,  he  married  and  set  up  in  business  for  himself. 
He  had  now  to  go  to  the  early  market  regularly  instead  of 
occasionally,  and  had  more  work.  This  he  did  pretty  well 
for  a  time,  but  he  soon  had  to  spare  himself,  and  his 
business  fell  off.  In  1875,  seven  years  from  the  time  he 
was  first  seen,  he  was  ill  at  home  with  rheumatism,  and  then 
lived  in  a  basement.  In  1880,  when  again  attacked  by 
rheumatism,  he  consented  to  enter  the  hospital  as  in-patient, 
which  he  had  refused  to  do  previously.  He  was  again  in 
the  hospital  for  sub-acute  rheumatism  from  March  5  to 
May  8,  1882.  The  rheumatism  quickly  subsided,  and  there 
was   no   pain  after  March  18 ;  he  had,   however,  a  severe 


144  HEART  DISEASE. 

cough.  During  his  convalescence,  the  kind  of  irregularity 
of  pulse  and  heart  beat  characteristic  of  cardiac  failure  in 
aortic  regurgitation  was  manifest ;  after  three  or  four 
regular  and  fairly  equal  beats,  a  weak  supplementary  beat 
would  follow  too  quickly,  or  while  perceptible  at  the 
heart  would  be  missing  at  the  wrist,  or  the  irregularity 
might  go  further  than  this  ;  sometimes  also  the  pulse  would 
reveal  two  distinct  efforts  of  the  ventricle  in  its  systole,  and 
have  the  "  bis  feriens  "  character.  Occasionally  he  had  a 
severe  attack  of  dyspnoea.  He  improved,  however,  and  after 
being  up  and  about  the  wards  for  some  time,  was  sent  to  a 
convalescent  hospital,  where  after  doing  well  and  gaining 
strength,  he  died  suddenly,  fourteen  years  after  he  was 
first  seen.  A  post-mortem  examination  revealed  old-stand- 
ing extensive  disease  of  the  valves,  which  had  in  effect 
ceased  to  exist  as  valves,  great  general  dilatation  of  the 
aorta,  some  thickening  of  the  mitral  flaps  and  shortening 
of  the  tendinous  cords,  extreme  dilatation  and  hypertrophy 
of  the  left  ventricle,  some  dilatation  and  hypertrophy  of 
the  right  ventricle  without  any  affection  of  the  valves 
of  this  side  of  the  heart.  The  weight  of  the  heart  was 
forty-two  and  a  half  ounces. 

But  even  in  young  subjects,  as  soon  as  marked  symptoms 
begin  to  present  themselves,  danger  is  at  hand ;  when  they 
are  not  habitually  present,  the  readiness  with  which  they 
are  induced  by  exertion  serves  as  a  dynamic  test  of  great 
prognostic  value.  Some  years  since,  I  examined,  within  a 
short  time  of  each  other,  two  boys  with  very  extensive 
aortic  incompetence,  attended  with  almost  the  maximum 
degree  of  dilatation  and  hypertrophy.  The  physical  signs 
could  only  tell  us  that  there  was  great  incompetence,  and 
great  compensatory  change  in  both,  but  in  the  one  the 
heart  was  readily  put  off  its  balance,  and  serious  symptoms 
were  induced  by  slight  exertion  ;  in  the  other,  this  was  not 
so.   The  prognosis  was,  therefore,  widely  different  in  the  two 


AORTIC  INCOMPETENCE.  145 

cases.     The  former  died  suddenly  three  years  after  I  first 
saw  him,  while  the  latter  did  not  die  till  ten  years  later. 

In  aortic  regurgitation,  acquired  late  in  life,  the  prognosis 
is  rarely  favourable.  Even  if  the  lesion  be  the  result  of 
acute  endocarditis,  and  therefore  stationary,  the  heart  is 
unable  to  undergo  adequate  hypertrophy,  and  efficient 
compensation  will  not  be  established.  But  after  middle 
age  acute  endocarditis  is  of  rare  occurrence,  and  the 
incompetence  will  usually  be  due  to  degenerative  changes 
in  the  valves ;  the  lesion  will  therefore  be  progressive, 
especially  if  the  arterial  tension,  the  primary  cause  in  all 
probability  of  the  trouble,  is  not  carefully  kept  down  by 
suitable  treatment.  The  prognosis  is  still  more  un- 
favourable if  the  affection  is  due  to  syphilitic  disease  of 
the  aorta  invading  the  valves. 


Prognosis  in  Aoetic  Kegukgitation  with  Stenosis. 

When  aortic  stenosis  gradually  becomes  established  in 
a  case  where  aortic  incompetence  already  exists  of  such 
severity  that  symptoms  are  readily  and  easily  induced,  it 
may  act  to  a  certain  degree  as  a  palliative  agent,  by  limiting 
the  amount  of  regurgitation  and  making  the  circulation 
more  equable  and  regular.  As  the  stenosis  makes  its 
effects  felt,  the  pulse  will  lose  to  a  great  extent  its  collapsing 
character,  and  the  artery  will  not  empty  so  completely 
between  the  beats.  The  heart  will  undergo  further  hyper- 
trophy, and  the  risk  of  undue  dilatation  will  be  diminished. 
Dyspnoea  will  be  less  readily  induced,  and  the  patient  will 
be  less  liable  to  syncopal  attacks. 

I  have  seen  several  cases  in  which  a  patient,  after  being 
in  imminent  danger  from  aortic  regurgitation,  has,  on  the 
supervention  of  aortic  stenosis,  been  enabled  to  enjoy  a  life 
of  comparative  comfort  for  many  years.  It  does  not  follow 
that  the  onset  of  aortic  stenosis  is  of  favourable  prognostic 

L 


146  HEAR!  DISEASE. 

import  in  all  cases  of  incompetence ;  it  is  only  when  the 
aortic  valves  are  severely  damaged  and  are  incapable   of 
checking  the  regurgitant  stream  in  any  effectual  degree 
that  this  holds  good,  and  when  the  patient  is  still  young 
enough  for  further  cardiac  hypertrophy  to  take  place. 

Treatment. 

Perhaps  more  can  be  done  to  prolong  life  and  postpone 
suffering  in  aortic  regurgitation  than  in  any  other  form  of 
valvular  disease ;  at  any  rate,  it  is  in  this  disease  that  the 
greatest  difference  can  be  made  by  care  on  the  one  hand 
and  imprudence  on  the  other.  A  patient  may  die  suddenly 
from  a  single  rash  act  who  might  have  lived  twenty  years, 
or  condemn  himself  by  a  single  imprudence  to  a  short  and 
suffering  existence  when  fair  health  and  many  years  of  life 
were  possible  for  him.  It  is  more  especially  shortly  after 
the  occurrence  of  the  lesion,  before  full  compensatory 
hypertrophy  has  had  time  to  take  place,  that  such  accidents 
are  likely  to  happen.  Hence  it  is  especially  important 
when  aortic  regurgitation  has  been  recently  established  in 
acute  rheumatism  that  prolonged  rest  should  be  insisted 
upon. 

Six  or  eight  weeks  in  bed,  and  after  this  rest  in  the 
recumbent  posture  for  another  month  or  six  weeks,  is 
advisable,  and  the  boy  should  not  go  to  school,  or  the  young 
man  to  business  for  another  six,  eight,  or  twelve  months, 
according  to  circumstances.  It  is  even  possible  that  a 
diastolic  murmur  may  completely  disappear,  and  with  it  all 
symptoms  of  aortic  incompetence,  when  due  care  of  this 
kind  has  been  taken. 

Not  uncommonly  incompetence  of  the  aortic  valves  is 
discovered  unexpectedly  at  an  interval  after  an  attack  of 
rheumatism  during  which  endocarditis  had  not  been 
suspected,  or  had  not  been  revealed  by  murmurs.     It  is  a 


AORTIC  INCOMPETENCE.  147 

most  important  and  useful  precaution,  therefore,  to  examine 
the  heart  at  intervals  for  some  time  after  rheumatic  fever, 
and  it  is  an  imperative  duty  to  do  so  when  there  has  been 
cardiac  complication  of  any  kind  or  degree. 

In  children,  as  the  articular  manifestations  of  rheu- 
matism are  usually  so  slight,  and  the  heart  is  so  frequently 
attacked,  an  examination  of  this  organ  should  never  be 
omitted  :  there  may  be  nothing  to  suggest  the  presence  of 
endocarditis  :  but  a  history  of  transient  pains  in  the  joints 
with  febrile  disturbance  should  at  once  arouse  suspicion, 
and  the  presence  of  rheumatic  nodules  is  almost  pathogno- 
monic of  cardiac  mischief  present  or  to  come.  Irreparable 
damage  to  the  heart  not  infrequently  results  from  a  child 
being  allowed  to  go  about  with  unsuspected  endocarditis. 

Caution  and  rest  are  necessary,  not  only  after  an  attack 
in  which  there  has  been  endocarditis  setting  up  aortic 
regurgitation,  but  also  after  a  febrile  attack  of  any  kind 
complicating  cases  of  aortic  incompetence.  Dilatation  is 
easily  induced  in  a  heart  weakened  by  fever  under  the 
continual  strain  to  which  the  left  ventricle  is  exposed,  and 
there  is  special  liability  to  sudden  death  during  the  period 
of  convalescence  from  acute  illness. 

On  the  other  hand,  provided  care  and  complete  rest  are 
insisted  on,  the  heart  may  actually  regain  lost  ground  from 
the  diminution  of  resistance  in  peripheral  circulation  due 
to  the  arterio-capillary  relaxation  attending  pyrexia.  In 
a  severe  case  of  aortic  regurgitation,  I  have  known  an  old- 
standing  mitral  regurgitation  from  secondary  dilatation  of 
the  left  ventricle,  disappear  for  some  time  under  these 
circumstances. 

The  risk  of  sudden  death  makes  it  imperative  that  the 
patient  suffering  from  aortic  disease  should  be  specially 
warned  against  over-exertion  and  hurry,  such  as  running 
to  catch  a  train  or  running  upstairs,  or  excessive  mental 
excitement  of  any  kind.     The  fatal  event  does  not  always 


148  HEART  DISEASE. 

take  place  during  the  exertion  or  excitement,  but  may  be 
postponed  till  the  next  day.  Periods  of  rest  from  time  to 
time  may  be  of  striking  service.  Whenever  exaggeration 
of  the  short  and  sudden  character  of  the  pulse  is  observed, 
especially  if  there  is  a  faltering  in  the  beat  now  and  then, 
and  still  more  when  the  apex  of  the  heart  is  found  to  be  re- 
ceding outwards,  and  the  beat  is  becoming'  diffuse,  the  recum- 
bent posture  should  be  enforced  for  some  two  to  six  weeks. 

As  compensation  fails  and  symptoms  become  more  con- 
tinuous and  severe,  they  will  arise  from  and  take  their  cha- 
racteristics from  one  of  two  causes  :  either  (1)  failure  on  the 
part  of  ;the  left  ventricle  to  maintain  a  sufficient  movement 
of  blood  in  the  capillaries,  or  (2)  backward  pressure  in 
the  veins,  the  result  of  right  ventricle  failure  secondary 
to  that  of  the.  left.  In  the  former  case,  sudden  death  from 
syncope  with  little  warning  or  apparent  cause  is  liable  to 
occur ;  failing  that,  there  may  be  sleeplessness  of  a 
peculiarly  harassing  kind,  or  painful  dyspncea,  unexplained 
by  any  interference  with  the  entry  of  air  into  the  lungs,  or 
by  want  of  aeration  of  the  blood.  The  face  will  be  pale  and 
have  an  anxious  and  suffering  expression ;  the  patient  will 
be  very  restless  and  weary.  Dropsy,  if  present,  will  be 
slight,  though  there  may  be  some  fluid  in  the  pleural 
cavities  with  oedema  of  the  bases  of  the  lungs. 

Under  these  circumstances  the  object  of  treatment  is  to 
sustain  the  failing  heart  by  nourishment,  stimulants,  and 
such  remedies  as  may  contribute  to  this  end — nux  vomica 
or  strychnia,  with  ammonia  and  ether,  to  which  belladonna  or 
atropin  often  makes  a  valuable  addition  ;  sometimes  digitalis 
may  be  of  service,  but  it  must  be  used  with  caution  ;  or 
strophanthus,  which  theoretically  ought  to  be  safer  as 
having  less  contractile  influence  on  the  arterioles.  Morphia 
hypodermically  is  often  of  the  greatest  possible  benefit, 
giving  quiet  sleep,  which  is  not  only  an  inexpressible 
comfort  to  the  sufferer,  but  frequently  recruits  the  strength, 


AORTIC  INCOMPETENCE.  149 

and,  by  rendering  the  recumbent  posture  possible,  so  far 
relieves  the  heart  that  it  proves  the  starting-point  for  a 
temporary  recovery.  Occasionally,  however,  a  patient,  after 
a  good  night's  rest  procured  in  this  way,  will  say  he  feels 
better,  sit  up  in  bed,  and  suddenly  fall  back  dead.  This 
danger  of  syncopal  attacks  should  be  explained  to  patients 
and  friends,  so  that  watchfulness  and  care  on  their  part  may 
guard  against  any  imprudent  effort  or  sudden  movement 
which  might  be  attended  with  such  fatal  consequences. 
Morphia  or  opium  administered  by  the  mouth  is  much 
less  effectual,  bromides  are  mostly  useless,  chloral  is 
positively  dangerous. 

Angina  pectoris  may  complicate  this  form  of  heart 
failure.  It  is  usually  relieved  by  nitrite  of  amyl  or  nitro- 
glycerine, and  patients  suffering  from  anginoid  pain  com- 
plicating aortic  regurgitation  may  come  to  take  the  latter 
remedy  in  extraordinary  doses.  When  relief  cannot  be 
obtained  in  any  other  way,  morphia  may  be  given  hypo- 
dermically.  Whatever  tends  to  strengthen  the  heart  or 
relieve  it  from  work  will  tend  to  prevent  the  onset  of 
anginoid  symptoms,  and  when  such  threaten,  treatment 
must  be  directed  to  these  two  points. 

Arsenic,  and  more  esjDecially  phosphorus,  have  had  in 
my  hands  a  very  beneficial  influence  as  cardiac  tonics  in  such 
cases. 

When  the  preponderating  character  of  the  symptoms 
is  that  of  venous  obstruction,  the  jugular  veins  being  dis- 
tended and  pulsating,  the  liver  enlarged,  and  dropsy  present ; 
when,  in  fact,  we  have  with  aortic  physical  signs  mitral 
symptoms,  the  line  of  treatment  is  quite  different  to  that 
just  described. 

Purgatives  should  be  given  in  full  doses,  but  judgment 
and  caution  must  be  exercised  in  their  administration,  as 
unfavourable  effects  may  develop  abruptly.  Digitalis  may 
then  be  given,  usually  with  great  benefit,  and  when  there 


ISO  HEART  DISEASE. 

is  much  dropsy,  diuretics  in  addition  to  the  digitalis  will 
often  have  a  marked  effect.  It  is  under  such  conditions 
that  digitalis  finds  its  opportunity  in  aortic  regurgitation, 
and  justifies  the  statements  of  those  who  find  this  remedy  of 
the  same  service  in  aortic  as  in  mitral  disease. 

If  the  administration  of  digitalis  is  persisted  in  after  the 
recovery  from  dropsy  and  the  more  severe  symptoms  of 
venous  stasis,  it  is  not  uncommon  for  patients  to  die 
suddenly,  sometimes  before  leaving  bed,  more  frequently 
when  they  have  begun  to  get  up  and  move  about.  There 
are  grounds  for  suspicion  that  digitalis  contributes  to  this, 
but  sudden  death  may  occur  whether  it  has  been  left  off  or 
not.  In  the  absence  of  mitral  symptoms,  it  is  rarely  that 
digitalis  is  called  for  in  aortic  incompetence  or  is  of  service, 
and  it  may  undoubtedly  do  harm.  It  may  set  up  sickness, 
which  is  an  ominous  symptom  in  this  form  of  disease,  and 
induces  a  condition  of  asthenia  difficult  to  remedy. 

Venesection,  even  when  the  venous  stasis  is  severe,  is 
rarely  to  be  contemplated.  It  is  true  that  the  relief  to  the 
right  ventricle  so  afforded  might  enable  it  to  regain  control 
over  its  contents  and  increase  the  supply  of  blood  to  the 
left  ventricle  and  the  amount  available  for  distribution  to 
the  arterial  system,  but  before  this  occurs  there  may  be  a 
momentary  faintness,  leading  to  a  fatal  attack  of  syncope. 


CHAPTER  XL 

MITRAL    INCOMPETENCE    OR   REGURGITATION. 

etiology  and  morbid  anatomy — physical  signs — the 
murmur  of  mitral  incompetence — the  pulse — 
explanation  op  irregularity  of  pulse — mitral 
incompetence  due  to  endocarditis— estimation 
of  extent  of  lesion,  from  character  of  murmur 
and  first  sound  and  from  compensatory  changes 
in  the  heart — symptoms — prognosis — mitral  in- 
competence without  damage  to  valves  —  its 
causation  and  explanation— differential  diag- 
nosis— treatment. 

Etiology  and  Morbid  Anatomy. 

The  causation  of  mitral  incompetence  is  most  varied. 
It  may  be  due  to  actual  damage  to  the  mitral  valve  by  acute 
or  chronic  endocarditis,  or  to  imperfect  apposition  of  the 
valves  or  stretching  of  the  orifice  from  dilatation  of  the 
left  ventricle.  The  former  group,  where  the  valves  have 
been  injured  by  an  inflammatory  process,  will  be  first  con- 
sidered. 

The  kind  and  degree  of  deformity  produced  by  endo- 
carditis may  vary  greatly.  The  edges  may  be  thickened 
and  shrunken,  presenting,  instead  of  the  translucent,  thin, 
flexible  curtain,  an  opaque,  inelastic,  rounded  border,  in 
which  the  delicate  marginal  ramifications  of  the  tendinous 
cords  are  swallowed  up  and  lost.    A  considerable  area  of  valve 


152  HEART  DISEASE. 

may  still  be  available  for  closing  the  orifice,  although  the 
apposition  may  not  be  accurate.  In  a  more  advanced  state 
of  change,  the  body  of  the  cusps  may  be  opaque,  thickened, 
and  contracted  so  that  a  considerable  gap  must  remain, 
allowing  of  great  reflux  even  when  their  approximation  is 
greatest ;  and  sometimes  this  is  carried  so  far  that,  as  valves, 
they  are  practically  non-existent,  especially  when  the 
chordae  tendinese  are  greatly  shortened,  which  they  may  be 
to  an  extent  which  brings  the  margins  of  the  flaps  close  to 
the  apices  of  the  papillary  muscles. 

Chronic  endocarditis  or  degenerative  change  may 
produce  some  opacity,  thickening,  and  deformity,  giving 
rise  to  insufficiency,  and  calcification  is  not  uncommon. 

Physical  Signs. 

The  Murmur. — The  evidence  of  regurgitation  through 
the  mitral  orifice  is  a  systolic  murmur  heard  in  the 
region  of  the  apex,  and  very  frequently  beyond  the  apex 
in  the  fifth  or  sixth  space  towards  the  axilla.  It  is 
often  audible  also  at  the  back  of  the  chest,  between  the 
scapula  and  the  spine,  at  about  the  middle  of  the  posterior 
border  of  the  scapula.  The  murmur  reaches  the  surface  at 
this  point,  not  by  extension  round  the  thorax  from  the 
axilla,  but  by  an  independent  route,  being  conducted  by 
the  vertebrae  from  the  base  of  the  ventricle,  the  shoulder 
of  which  rests  upon  the  spinal  column.  Occasionally 
the  murmur  of  mitral  regurgitation  is  heard  more  loudly 
in  the  fourth  or  even  in  the  third  space  in  the  vertical  nipple 
line  or  just  outside  it,  than  at  the  apex.  When  this  is 
the  case,  an  impulse  is  usually  to  be  felt  at  or  near  the 
same  point. 

Murmurs  which  may  be  mistaken  for  Mitral  Regurgitant 
Murmur.— The  only  murmurs  likely  to  be  mistaken  for  this 
are,  a   systolic   aortic   murmur  conducted  to   the   apex,  a 


MITRAL   INCOMPETENCE.  153 

systolic  and  therefore  regurgitant  tricuspid  murmur,  and 
the  spurious  murmur  produced  by  compression  of  the  edge 
of  the  lung  by  the  ventricular  systole.  A  pulmonic  systolic 
murmur  is  also  occasionally  heard  almost  at  the  apex.  A 
question  which  frequently  arises  when  a  systolic  murmur 
is  heard  both  at  the  base  and  at  the  apex,  is,  whether 
it  is  one  and  the  same,  in  which  case  it  will  be  aortic, 
or  whether  it  arises  from  two  independent  sources.  It  is 
only  when  the  murmur  is  loudest  over  the  aorta  that  there 
can  be  any  uncertainty,  and  as  a  rule  it  is  not  difficult  to 
decide.  Any  marked  difference  in  the  tone  or  character  of 
the  apex  murmur,  as  compared  with  that  heard  at  the  base, 
or  a  superadded  musical  element  in  it,  would  be  sufficient 
to  show  that  it  was  not  the  conducted  aortic  murmur,  and 
where  such  evidence  as  this  is  lacking,  if  the  apex  murmur 
is  longer  than  the  aortic,  and  especially  if  it  is  conducted 
outwards  for  any  distance,  or  is  heard  in  the  left  inter- 
scapular space,  there  can  be  no  doubt.  It  must  be 
remembered,  however,  that  a  loud,  rough,  aortic  murmur 
may  be  heard  as  a  smooth  murmur  of  a  different  tone  at  the 
apex,  the  thick  muscular  wall  of  the  ventricle  not  lending 
itself  to  the  propagation  of  coarse  vibrations,  which  are, 
in  fact,  vibrations  of  the  aorta  itself.  A  loud  aortic 
murmur,  again,  may  be  audible  all  down  the  thoracic  spine. 
With  regard  to  the  tricuspid  murmur  a  special  warning 
may  be  of  service,  as  it  is  not  unfrequently  set  down  as 
mitral.  The  tricuspid  area,  so  called,  is  over  the  lower 
costal  cartilages,  near  the  ensiform  appendage,  but  a 
systolic  tricuspid  murmur  is  often  heard  as  far  out  as  the 
apex,  and  occasionally  has  its  maximum  intensity  just  to 
the  inner  side  of  the  apex.  When  a  murmur  heard  at  the 
apex  is  lost  immediately  to  the  left  of  the  beat,  while  it  is 
audible  between  the  apex  and  the  lower  end  of  the  sternum, 
its  seat  of  production  is  at  the  tricuspid,  and  not  at  the 
mitral  orifice. 


154  HEART  DISEASE. 

An  imitation  of  a  systolic  apex  murmur  is  not  un- 
frequently  produced  by  movement  of  air  in  the  lungs 
overlapping  the  heart  as  it  is  compressed  by  the  systole  of 
the  heart,  and  it  is  sometimes  loud  enough  to  be  heard  by 
the  subject.  The  imposture  is  easily  detected,  by  the  fact 
that  it  is  only  audible,  as  a  rule,  during  inspiration,  or  is,  at 
any  rate,  much  more  distinct  then,  and  that  its  distribution 
does  not  coincide  with  the  conduction  of  the  true  mitral 
murmur,  but  follows  the  line  of  the  thin  edge  of  the  lung 
across  the  pericardium  from  the  neighbourhood  of  the  apex 
towards  the  sternum. 

The  sources  of  error  just  mentioned  being  eliminated,  a 
systolic  murmur  audible  at  and  to  the  left  of  the  apex,  is 
mitral  in  origin,  and  indicates  incompetence  in  the  valve 
and  reflux  of  blood  into  the  left  auricle.  There  is  not  the 
same  doubt  as  to  its  significance  as  there  is  with  regard 
to  the  constant  association  of  obstruction  with  an  aortic 
systolic  murmur ;  a  mitral  systolic  murmur  means  regurgi- 
tation. It  does  not,  however,  necessarily  imply  that  there 
is  actual  disease  of  the  mitral  valve,  as  there  are  other 
causes,  enumerated  later,  which  may  give  rise  to  mitral 
regurgitation  from  dilatation  of  the  left  ventricle  or 
stretching  of  the  mitral  orifice. 

The  Pulse. — The  distinguishing  characteristic  is  irregu- 
larity, both  in  rhythm  and  in  force.  In  advanced  cases  no 
two  beats  are  alike;  a  few  fairly  strong,  full  pulsations, 
at  something  like  proper  intervals,  will  be  followed  by  a 
number  of  feeble,  hurried  beat's,  these  again  perhaps  by 
a  single  good  stroke,  after  which  there  is  a  pause  and  then 
renewed  hurried  action.  Little  difference  of  opinion  exists 
as  to  the  association  of  mitral  incompetence  with  irregu- 
larity of  pulse.  It  would  not  be  true  to  assert  that  there 
can  be  no  considerable  regurgitation  without  irregular 
action  of  the  heart,  but  it  is  a  safe  working  hypothesis  that 
a  mitral  murmur  is  not  attended  with  serious  reflux  while 


MITRAL  INCOMPETENCE.  155 

the  pulse  remains  regular.  What,  then,  is  the  cause  of  the 
irregularity?  We  find  similar  irregularity  occasionally 
attending  dilatation  of  the  heart,  and  it  might  be  suggested 
that,  as  mitral  insufficiency  is  not  unfrequently  the  result 
of  dilatation  of  the  ventricle,  the  irregularity  of  the  pulse 
is  symptomatic  of  the  dilatation,  and  not  of  the  regurgi- 
tation ;  but  the  irregularity  accompanies  incompetence 
caused  by  rheumatic  damage  of  the  valves,  quite  as 
constantly  as  it  does  the  insufficiency  due  to  dilatation. 

Irregular  heart  action  and  pulse,  again,  may  be  among 
the  final  symptoms  in  any  form  of  valvular  disease,  though 
they  are  rarely  quite  of  the  same  character  as  in  mitral 
regurgitation ;  but  in  this  latter  disease  the  irregularity 
supervenes  early,  and  is  not  inconsistent  with  fair  compensa- 
tion and  apparent  health  for  many  years. 

It  is  probable  that  the  varying  pressure  to  which  the 
heart  is  subjected  in  inspiration  and  expiration  may  account 
for  it.  The  variations  of  intrathoracic  pressure  in  ordinary 
respiration  have  no  obvious  effect  on  the  action  of  the 
heart ;  but  we  can  at  any  time  slightly  disturb  the  rhythm 
of  the  heart  and  pulse  by  taking  and  holding  a  very 
deep  breath.  When  again  there  is  incipient  irregularity 
careful  observation  will  almost  always  show  that  the  break 
in  the  rhythm  occurs  at  the  moment  when  there  is  a 
change  in  the  intrathoracic  pressure  at  the  beginning  and 
end  of  inspiration  or  expiration.  This  is  best  seen, 
perhaps,  in  cases  of  bronchitis  and  emphysema  with  dilated 
right  heart.  The  thin-walled  auricles  will  be  all  the  more 
susceptible  of  this  change  of  pressure  when  distended  and 
dilated,  while  it  will  scarcely  affect  the  ventricles. 

The  heart  works  habitually  under  a  negative  pressure  due 
to  the  elastic  traction  of  the  lungs,  and  is  only  subjected 
to  positive  pressure,  strictly  speaking,  when  the  chest  is 
filled  and  the  glottis  closed  in  effort.  The  aspiration  re- 
sulting from  the  negative  pressure  is  greatest  in  inspiration, 


156  HEART  DISEASE. 

and  aids  the  circulation  by  drawing  the  blood  into  the 
auricles,  which  then  carry  it  on  into  the  ventricles.  In 
expiration  the  auricles  are  more  or  less  compressed  as  the 
chest  walls  collapse. 

When  the  left  auriculo-ventricular  valves  are  incom- 
petent, the  pressure  on  the  auricle  during  expiration  will 
aid  in  resisting  the  systolic  reflux  from  the  ventricle,  and 
in  driving  the  blood  into  the  ventricle  during  diastole  ;  at 
the  moment  when  the  positive  pressure  of  expiration  is 
exchanged  for  the  negative  pressure  of  inspiration,  the 
resistance  to  the  reflux  of  blood  into  the  auricle  is  suddenly 
diminished,  so  that  more  will  be  allowed  to  regurgitate,  and 
less  will  be  carried  into  the  aorta,  and  there  will  be  no 
compression  of  the  auricle  to  aid  in  filling  the  ventricle. 
Corresponding  differences  of  an  opposite  kind  will  attend 
the  end  of  inspiration.  The  varying  supply  of  blood  to  the 
ventricle  thus  induced,  cannot  fail  to  produce  a  tendency  to 
irregularity. 

Estimation  of  the  Extent  of  the  Lesion. — Our  first  inquiry 
will  be  as  to  the  physical  signs  and  symptoms  by  means 
of  which  we  may  approximately  infer  the  degree  of  impair- 
ment of  the  valves,  and  the  amount  of  regurgitation  which 
takes  place. 

The  murmur  affords,  in  some  cases,  important  informa- 
tion. When  it  is  not  conducted  much  beyond  the  situation 
of  the  apex  beat,  the  apex  itself  not  being  greatly  displaced, 
and  is  not  audible  in  the  back,  the  regurgitation  is  usually 
slight.  But  an  exception  to  this  statement  may  be  found 
at  the  opposite  extreme,  when  the  orifice  is  gaping  and  the 
ventricle  weak.  Under  such  circumstances  the  murmur  may 
be  short  and  scarcely  audible  ;  symptoms,  however,  will  at 
once  distinguish  between  the  two  conditions. 

The  persistence  of  the  left  ventricle  first  sound  is 
evidence  that  there  is  no  advanced  change  in  the  valves, 
more  especially   when   the  murmur   is   retarded.     This   is 


MITRAL   INCOMPETENCE.  157 

an  important  point  to  note.     If  the  regurgitation  is  con- 
siderable, the  murmur  takes  the  place  of  the  first  sound, 
and  is  said  to  hide  it ;  but  it  is  not  a  mere  question  of 
loudness,  there  is  a  true  substitution  of  the  murmur  for  the 
sound.     When,  therefore,  the  first  sound  is  distinctly  heard 
heading  the  murmur,  some  difference  exists.     It  would  be 
going  too  far  to  say,  as  in  the  case  of  the  aortic  valves,  that 
the  sound  indicates  sufficient  check  to  the  refluent  blood  to 
produce  tension  of  the  valves  and  cords,  and  of  the  ventri- 
cular wall,  but  the  inference  tends  in  that  direction.     With 
regard   to  the   retarded-systolic  mitral  murmur,  when  the 
murmur  follows  the  first  sound  at  a  distinct  though  very  brief 
interval,  it  would  seem  that  there  is,  in  the  first  instance, 
complete  closure  of  the  valves,  but  that  during  the  contrac- 
tion of  the  ventricle,  the  apposition  is  deranged   so   that 
leakage  occurs.     Such  leakage  can  scarcely  be  other  than 
slight.    These  inferences  are  confirmed  by  the  fact  that  the 
persistent  first  sound  and  the  retarded  systolic  murmur  are 
most  common  in  the  curable  or  temporary  regurgitation  of 
ansemia,  and  the  conclusions  based  on  this  observation  may 
be  extended  to  other  cases  than  those  of  early  life.     One 
caution    is   necessary,    that   is,  to    beware    of   taking    the 
modified  short,  sharp,  first  sound  of  mitral  stenosis,  when 
there  is  both  obstruction  and  regurgitation,  for  the  normal 
second  sound. 

The  general  statement  made  in  the  first  chapter  that  a 
loud  and  long  murmur  is  usually  significant  of  a  lesser 
degree  of  structural  damage  and  functional  imperfection 
than  a  short  and  weak  murmur,  is  another  point  to  be  borne 
in  mind.  Loudness  implies  strength  of  contraction,  and 
length  shows  that  the  ventricle  goes  through  with  its 
systole,  and  also  that  it  is  not  quickly  emptied,  as  it  would 
be  were  there  a  large  escape  into  the  auricle.  The  murmur 
of  worst  significance  is  a  short,  weak  whiff,  varying  in 
intensity  and  duration  in  successive  beats. 


158  HEART  DISEASE. 

It  is  the  mitral  systolic  murmur  which  is  most  frequently 
musical ;  very  commonly,  but  not  perhaps  always,  the 
musical  murmur  indicates  a  narrow  chink,  and  therefore 
little  reflux.  The  musical  note  may  be  high-pitched  or  low, 
nearly  always  it  is  accompanied  by  a  blowing  murmur,  and, 
according  to  my  experience,  has  never  the  pure  tone  some- 
times produced  at  the  aortic  orifice.  It  does  not  always 
begin  at  the  same  time  with  the  blowing  murmur,  but  may 
be  interpolated  into  it,  beginning  later  and  ending  sooner. 

As  the  action  of  the  heart  is  frequently  irregular,  the 
intensity,  character,  pitch,  and  length  of  the  murmur  may 
vary  from  one  beat  to  another. 

For  further  evidence  we  must  trace  the  effects  of  regur- 
gitation through  the  mitral  orifice.  The  immediate  effect  of 
reflux  of  blood  into  the  left  auricle  will  be  to  distend  this 
cavity,  but,  lying  deeply  as  it  does,  the  physical  signs  of 
an  early  stage  of  dilatation  are  not  such  as  can  be  relied 
upon  for  definite  information ;  but  another  result  which 
follows  early  is  obstruction  to  the  free  outflow  of  blood 
from  the  pulmonary  veins  into  the  auricle,  and  this  soon 
makes  itself  felt  backwards  through  the  capillaries  of  the 
lungs,  and  gives  rise  to  high  pressure  in  the  pulmonary 
artery.  Here  we  come  upon  audible  evidence ;  the  in- 
creased tension  brings  down  the  semilunar  valves  with 
greater  force,  and  gives  rise  to  accentuation  of  the  pul- 
monic second  sound.  It  is  not  easy  to  say  what  degree  of 
intensification  of  this  second  sound  is  required  as  proof  of 
obstruction  to  the  flow  of  blood  through  the  lungs.  The 
aortic  second  sound  has  to  be  taken  as  a  basis  for  com- 
parison, and  while  most  observers  say  that  the  aortic  is  the 
louder  of  the  two,  my  own  conclusion  is  that  the  pulmonic 
is  usually  louder  than  the  aortic.  Again,  the  pulmonic 
second  sound  may  be  accentuated  by  resistance  arising  in 
the  lungs  themselves,  as  in  bronchitis  and  emphysema. 
Marked    and    persistent    intensification    of    the   pulmonic 


MITRAL   INCOMPETENCE.  159 

second  sound,  when  a  mitral  systolic  niurmur  is  present, 
must,  however,  be  taken  as  evidence  of  sufficient  reflux  to 
increase  the  pressure  in  the  pulmonary  artery  by  the 
obstruction  to  which  it  gives  rise. 

Changes  in  the  Heart.— From  this  follow  hypertrophy 
and  dilatation  of  the  right  ventricle.  The  call  upon  the 
right  ventricle  for  increased  force  in  propelling  the  blood 
through  the  lungs  results  in  a  combination  of  dilatation 
and  hypertrophy,  of  which  the  physical  signs  are  displace- 
ment of  the  apex  outwards  or  to  the  left  and  undue  right 
ventricle  impulse,  felt  when  the  hand  is  placed  over  the 
lower  costal  cartilages  to  the  left  of  the  sternum,  and  seen, 
and  perhaps  felt,  in  the  epigastrium  and  below  the  left 
costal  margin.  The  right  ventricle  in  effect  comes  to  the 
aid  of  the  left ;  the  heightened  pressure  maintained  by  its 
means  in  the  left  auricle  resists  the  reflux  of  blood  from 
the  ventricle,  and  since  life  is  often  sustained  when  the 
valves  are  practically  non-existent,  the  intra-auricular 
pressure  must  in  such  cases  almost,  if  not  quite,  equal  the 
pressure  in  the  systemic  arteries.  Further,  the  same  force 
which  resists  the  reflux  must,  on  the  relaxation  of  the  left 
ventricle,  drive  the  blood  violently  into  it,  taking  it,  so  to 
speak,  at  a  disadvantage,  and  distending  it  in  the  same 
way,  though  not  to  the  same  degree,  as  aortic  regurgitation, 
giving  rise  thus  to  dilatation,  which  is  accompanied  or 
followed  by  more  or  less  hypertrophy.  In  proportion  as 
the  left  ventricle  is  enlarged,  the  apex  will  be  carried 
downwards  and  its  beat  become  conspicuous,  and  the  hyper- 
trophy of  the  right  ventricle  pushing  it  outwards  and  some- 
times upwards,  the  ultimate  displacement  of  the  apex  will 
be  the  resultant  of  the  changes  in  the  two  ventricles. 
There  will  also  be  dilatation  of  the  auricles.  The  volume 
of  the  heart  as  a  whole  will  thus  be  increased,  giving 
rise  to  a  corresponding  extension  of  the  area  of  deep 
dulness. 


160  HEART  DISEASE. 

These  changes,  the  necessary  result  of  the  incompetence 
of  the  mitral  valve,  traceable  directly  to  the  mechanical 
difficulty  produced  by  it,  become  the  measure  of  the  diffi- 
culty and  of  the  incompetence.  A  systolic  mitral  murmur 
without  increase  in  the  area  of  cardiac  dulness,  without 
much  displacement  of  the  apex,  and  without  marked 
accentuation  of  the  pulmonic  second  sound,  without,  again, 
symptoms  indicative  of  disturbance  of  the  circulation  such 
as  might  be  due  to  failure  in  the  compensatory  changes,  is 
not  attended  with  any  considerable  regurgitation,  and  is  not 
a  source  of  present  danger.  Unless  there  is  reason  to  look 
upon  it  as  the  beginning  of  progressive  damage,  it  may 
practically  be  disregarded.  As  the  signs  of  pressure  in  the 
pulmonary  circulation  and  of  changes  in  the  walls  and 
cavities  of  the  heart  increase,  we  infer  increase  in  the 
amount  of  reflux,  for  they  indicate  greater  difficulty  in 
neutralizing  its  injurious  effects.  We,  therefore,  calculate 
on  diminished  stability  of  the  compensatory  balance  and 
on  less  power  of  regaining  a  working  equilibrium  of  the 
circulatory  forces  if  it  is  once  overthrown. 

To  sum  up  the  indications  by  which  the  extent  of  the 
lesion  may  be  surmised  : 

While  it  may  safely  be  said  that  if  the  pulse  remains 
regular  the  reflux  is  slight,  the  degree  of  irregularity  of 
the  pulse  will  not  be  any  criterion  as  to  the  extent  of  the 
reflux.  More  is  to  be  learnt  from  the  degree  of  vigour  of 
the  beat,  and  the  length  of  the  pulse  wave. 

Further  information  will  be  derived  from  the  character 
of  the  murmur,  and  the  extent  to  which  it  replaces  the 
first  sound,  and  again  from  accentuation  of  the  pulmonic 
second  sound  ;  but  the  amount  of  dilatation  and  hyper- 
trophy of  the  heart,  more  especially  of  the  right  ventricle, 
will  afford  a  more  accurate  basis  for  the  estimation  of  the 
degree  of  incompetence.  The  symptoms  must  also  be  con- 
currently taken  into  consideration. 


mitral  incompetence.  161 

Symptoms. 

No  symptoms  will  be  present  in  cases  of  slight  regur- 
gitation even  on  moderate  exertion.  In  more  severe  cases, 
or  when  compensation  is  beginning  to  fail,  shortness  of 
breath,  a  tendency  to  cyanosis,  and  slight  pitting  of  the 
legs  at  night  will  be  among  the  earliest  symptoms.  The 
dyspnoea  and  cyanosis  will  become  more  marked  and  per- 
sistent as  time  goes  on,  and  are  due  to  congestion  and 
passive  hyperemia  in  the  lungs  from  back  pressure  in  the 
pulmonary  circulation,  which  gives  rise  to  the  secondary 
changes  in  the  lungs  described  in  the  chapter  on  mitral 
stenosis.  The  pressure  in  the  pulmonary  circulation,  how- 
ever, is  not  so  high  as  in  mitral  stenosis,  and  hsemioptysis 
does  not  occur  in  pure  mitral  incompetence,  nor  is  the  con- 
dition of  brown  induration  so  definitely  established.  The 
tendency  is  rather  to  congestion  and  oedema  of  the  bases 
of  the  lungs  than  to  fibrosis,  and  cough  is  often  a  trouble- 
some symptom,  the  more  so  as  the  patient  is  especially 
liable  to  attacks  of  bronchitis.  (Edema  of  the  legs  is  a 
comparatively  early  symptom,  but  is  at  first  readily 
amenable  to  treatment  by  rest  in  bed  and  suitable 
medicaments.  The  liver  enlarges  as  the  right  ventricle  is 
unable  to  cope  efficiently  with  the  effects  of  the  mitral  lesion, 
and  its  varying  size  is  therefore  an  important  indication  as 
to  the  efficiency  of  compensation.  It  will  pulsate  when 
tricuspid  incompetence  is  established,  but,  as  a  rule,  it 
feels  less  firm  and  hard  than  in  mitral  stenosis,  and  ascites 
is  less  common. 

The  morbid  anatomy  of  the  secondary  changes  in  the 
lungs  and  liver  in  mitral  disease  are  described  in  the 
chapter  on  mitral  stenosis. 

Prognosis. 
The  range  of  possibilities  as  regards  duration  of  life  in 
mitral  regurgitation,  due  to  actual  damage  of  the  valve  by 

M 


162  HEART  DISEASE. 

acute  endocarditis,  is  more  extensive  than  in  any  other  form 
of  valvular  disease.  It  is  the  least  serious  and  the  most 
amenable  to  treatment  of  all  the  valvular  affections. 

When  the  lesion  is  slight  the  patient  may  live  to  old 
age  without  experiencing  inconvenience  from  the  results  of 
the  leakage,  and  may  be  capable  of  much  hard  work  and  pass 
through  serious  illnesses.  In  moderately  severe  cases,  with 
reasonable  precautions,  he  may  live  many  years  without 
serious  symptoms  declaring  themselves.  Women  with 
mitral  regurgitation  may  bear  children  with  impunity. 

In  endeavouring  to  forecast  the  further  course  of  a  case 
of  mitral  incompetence  when  the  regurgitation  is  incon- 
siderable, or  when  compensation  has  been  established,  one 
of  the  most  important  considerations  will  be  the  degree 
of  arterial  tension.  Everything,  so  to  speak,  will  depend 
upon  the  amount  of  resistance  in  the  peripheral  systemic 
circulation,  and  this  may  vary  extremely.  If  with  a  given 
degree  of  mitral  incompetence,  we  have  undue  arterial 
tension,  the  force  of  the  regurgitant  stream  will  be  great, 
the  back  pressure  in  the  auricle  and  pulmonary  circulation 
high,  the  demand  upon  the  right  ventricle  severe,  all  of 
which  are  circumstances  tending  to  the  production  of 
structural  changes ;  if,  on  the  other  hand,  the  arterial 
tension  is  low,  the  conditions  are  reversed. 

The  case  of  a  patient,  whom  I  have  known  to  have 
mitral  regurgitation  for  at  least  thirty-five  years,  may 
illustrate  this.  When  first  seen  there  were  disquieting 
symptoms,  a  sense  of  constriction  and  oppression  at  the 
chest  on  moderate  exercise,  and  liability  to  slight  fainting 
attacks.  Finding  with  such  symptoms  the  pulse  ex- 
tremely short,  soft,  and  compressible,  it  was  at  first  feared 
that  there  were  degenerative  changes  in  the  heart,  but  the 
family  pulse,  as  exhibited  by  several  children  and  grand- 
children, Avas  one  of  extremely  low  tension,  and  this  was 
found  to  be  the  explanation  of  the  patient's  weak  pulse. 


MITRAL    INCOMPETENCE.  163 

There  can  be  no  doubt  that  the  absence  of  resistance  in  the 
systemic  arterioles  and  capillaries  had  an  important  share  in 
the  prolonged  immunity  from  structural  changes  which  he 
has  enjoyed  in  spite  of  work  of  the  most  trying  and 
arduous  kind. 

One  or  two  other  examples  of  prolonged  survival  may 
be  mentioned.  Two  gentlemen,  in  whom  I  found  mitral 
regurgitation  more  than  twenty  years  since,  were,  when  I 
last  saw  them,  more  than  forty  years  of  age  and  in  active 
work.  The  murmur  was  loud  and  long  in  both,  and  in 
one  there  was  considerable  hypertrophy  of  the  right  ventri- 
cle and  marked  irregularity  of  the  pulse.  Another  gentle- 
man, whom  I  have  repeatedly  examined,  and  found  to  have 
a  mitral  systolic  murmur,  was,  thirty-five  years  before  I 
saw  him,  condemned  to  life-long  inactivity,  and  I  learnt 
from  the  family  medical  man  that  there  had  been  a  con- 
tinuous history  of  valvular  disease  for  that  length  of  time  ; 
he  rebelled  against  the  sentence,  and  was  still  at  the 
age  of  sixty-four  doing  strenuous  work.  Nothing  is  more 
common  than  to  find  a  mitral  systolic  murmur  after  the  age 
of  seventy,  but  we  cannot  say  how  long  it  has  been  present, 
as  it  is  not  often  that  we  can  date  it.  Mitral  regurgitation 
is  the  disease  which  sends  patients  into  hospital  time  after 
time,  often  with  advanced  dropsy  or  severe  pulmonary 
complication,  from  which  they  recover  so  completely  as  to 
resume  work  for  a  while.  It  is  again  the  affection  most 
commonly  met  with  in  out-patient  hospital  practice,  while 
among  in-patients  and  in  the  post-mortem  room  it  is  less 
frequently  represented  than  mitral  stenosis.  All  these  facts 
point  to  one  conclusion,  viz.  that  mitral  incompetence  is 
not  a  deadly  form  of  heart  disease  ;  I  consider  it  to  be  less 
serious  than  aortic  stenosis.  It  is  not  merely  that  in  a 
large  number  of  cases  the  actual  damage  to  the  valve  and 
the  consequent  functional  imperfection  is  only  slight,  but 
there  is  ample  provision  for  compensatory  adjustments,  and 


1 64  HEART  DISEASE. 

very  extensive  change,  if  it  is  stationary,  may  be  survived 
twenty  or  thirty  years,  and  not  prevent  the  patient  reaching 
old  age  in  comfort. 

Mitral  Incompetence  without  Damage  to  Yalves. 

In  the  large  group  of  cases  of  mitral  regurgitation  now 
to  be  considered,  the  cause  of  the  reflux  is  not  actual 
damage  to  the  mitral  valves,  but  stretching  of  the  orifice 
or  imperfect  closure  of  the  valves,  due  to  dilatation  of  the 
left  ventricle. 

Such  dilatation  may  be  secondary  to  aortic  disease,  or 
the  result  of  prolonged  high  arterial  tension ;  but  mitral 
regurgitation  due  to  these  causes  need  not  be  considered 
here,  as  its  prognosis  and  treatment  are  those  of  the  primary 
affection,  and  have  been  discussed  elsewhere. 

The  chief  causes  of  mitral  incompetence  in  the  group 
to  be  considered,  are :  anaemia,  acute  febrile  disorders,  and 
conditions  associated  with  advancing  age. 

The  so-called  hseinic  mitral  murmurs  which  have  some- 
times been  supposed  to  have  some  other  significance  than 
actual  reflux,  as  they  disappear  with  improving  health, 
are  not  unfrequently  met  with  in  anseinia,  especially  in 
young  women,  or  at  times  after  acute  febrile  diseases,  such 
as  acute  rheumatism,  typhoid  fever,  or  measles  ;  the  systolic 
mitral  murmurs  so  commonly  present  in  chorea  sometimes 
belong  to  the  same  class,  and  mitral  regurgitation,  coming 
on  late  in  life,  not  unfrequently  has  a  similar  causation, 
although  it  may  not  be  removed  by  treatment. 

It  is  to  all  this  class  of  cases  that  McAlister's*  explana- 
tion of  mitral  reflux  without  disease  of  the  valves  or  en- 
largement of  the  orifice,  already  referred  to,  applies.  It 
had  been  forgotten  or  overlooked,  notwithstanding  ocular 
demonstration     on    the     living    heart,    and     preparations 

*  British  Medical  Journal,  August,  18S2. 


MITRAL  INCOMPETENCE.  165 

showing  the  heart  in  systole  and  diastole  by  Sibson, 
notwithstanding  also  measurement  of  the  circumference 
of  the  heart  in  the  contracted  and  relaxed  condition  and 
the  fact  that  the  opening  was  only  the  upper  end  of 
the  ventricular  cavity,  that  contraction  of  the  orifice  con- 
tributed in  an  important  degree  to  its  perfect  closure  by  the 
valves.  When  regurgitation  occurred,  which  was  not  ex- 
plained by  changes  in  the  valves,  it  was  accounted  for  by 
irregular  action  of  the  papillary  muscles,  or  by  the  sup- 
position that  the  papillary  muscles,  and  with  them  the 
tendinous  cords,  were  carried  by  dilatation  of  the  ventricle 
to  such  a  distance  from  the  base  of  the  valves  that  the 
margins,  being  dragged  down  by  the  chordae  tendineae, 
could  not  meet.  It  was  demonstrated  in  McAlister's 
paper,  that  all  that  is  required  in  order  that  the  reflux  in 
question  may  occur,  is  that  from  languid  contraction  of  the 
cardiac  muscular  fibres,  or  from  resistance  in  the  peripheral 
circulation,  the  due  constriction  of  the  orifice  should  not 
take  place  ;  the  valvular  mechanism  will  then  be  deranged 
and  the  apposition  of  the  flaps  be  incomplete.  It  must  be 
added,  however,  that  if  the  contraction  of  the  orifice  is 
imperfect,  so  will  be  the  ventricular  systole  as  a  whole,  so 
that  the  position  of  the  papillary  muscles  may  contribute 
to  the  derangement. 

The  mitral  murmur  of  anaemia,  though  only  a  particular 
case  of  regurgitation  from  dilatation,  is  worthy  of  separate 
consideration.  It  is  met  with  in  only  a  small  proportion 
of  cases  of  anaemia,  and  may  be  absent  when  the  blood- 
lessness  is  extreme.  It  does  not,  therefore,  mark  a  certain 
degree  of  impoverishment  of  the  blood,  and  may  indeed  be 
found  when  this  is  by  no  means  advanced.  The  remarks 
apply  equally  to  chlorotic  anaemia,  to  anaemia  from  loss  of 
blood,  and  to  pernicious  anaemia.  The  fact  that  a  mitral 
murmur  is  so  often  absent  in  fatal  pernicious  anaemia  is 
perhaps  the  most  remarkable.     It  seems  probable  that  while 


166  HEART  DISEASE. 

the  poverty  of  the  blood  and  the  consequent  innutrition 
of  the  heart  are  the  predisposing  influences,  the  proximate 
cause  is  some  overstrain,  Avhich  may  be  sufficient  even  in 
the  absence  of  anaemia. 

As  an  instance  of  this,  may  be  quoted  the  case  of  a  young 
lady  whom  I  saw  from  time  to  time  during  a  period  of  four 
years.  She  was  well  nourished,  with  well-developed  muscles, 
as  well  as  a  fair  amount  of  adipose  tissue,  and  the  lips  and 
face  were  a  good  colour.  When  first  seen  she  had  a  pro- 
nounced mitral  murmur,  and  the  apex  beat  was  displaced  to 
the  left  of  the  nipple  line.  There  were  no  murmurs  in  the 
neck  or  over  the  pulmonic  area  or  aorta ;  the  catamenia 
were  excessive. 

This  was  her  condition  in  July ;  in  October  the  murmur 
had  disappeared  and  the  apex  had  receded.  In  the  following 
January,  after  the  death  of  a  relation  by  drowning,  which 
she  witnessed,  the  murmur  and  dilatation  had  returned. 
A  month  later  the  murmur  could  not  be  heard,  but  the 
apex  was  still  outside  its  normal  situation.  On  examina- 
tion in  July,  September,  and  December  of  that  year,  the 
apex  beat  was  normal  and  the  murmur  absent,  although 
the  menses  were  suspended  for  long  periods,  and  she  had 
lost  flesh.  No  further  relapse  had  occurred  when  I  last 
saw  her.  The  influences  which  appeared  to  determine  the 
occurrence  of  the  regurgitation  were  the  relaxing  climate 
in  which  her  home  was  placed ;  the  frequent  necessity,  from 
the  situation  of  the  house,  of  walking  uphill  when  tired  ; 
and,  probably  more  than  all,  domestic  worry. 

There  is,  however,  in  anaemia,  a  cause  of  dilatation  of 
the  weakened  left  ventricle  independent  of  external  and 
accidental  circumstances ;  this  is  high  arterial  tension, 
which,  as  has  been  elsewhere  pointed  out,  nearly  always 
attends  this  state  of  the  blood.  Undue  arterial  tension 
implies  increased  resistance  to  the  emptying  of  the  ventricle, 
and  this  gradually  distends  it.     When  regurgitation  is  not 


MITRAL   INCOMPETENCE.  167 

produced,  there  are  still  very  frequently  the  signs  of 
dilatation  in  displacement  outwards  and  downwards  of  the 
apex,  and  a  diffuse  character  of  its  beat.  The  operation  of 
this  cause  perhaps  throws  light  on  the  production  of 
permanent  valvular  disease  by  anaBinia,  which  G-oodhart  has 
shown  to  be  probable.  The  peripheral  resistance  throws 
extra  stress  upon  the  mitral  valves,  the  action  of  the  heart 
is  liable  to  be  excited  and  violent  in  anaemic  subjects,  which 
will  intensify  the  effects  of  the  strain,  and  so  valvulitis  may 
be  set  up. 

Differential  Diagnosis. 

It  may  sometimes  be  difficult  to  decide  whether  a  mitral 
murmur  is  due  to  conditions  such  as  have  just  been  described, 
or  to  actual  changes  in  the  valves.  Where  there  are 
obvious  compensatory  changes  in  the  left  or  right  ventricle, 
there  can  be  no  doubt,  and  in  many  cases  the  state  of  health 
of  the  patient  with  the  history  will  be  a  sufficient  guide ; 
but  difficulties  may  arise,  for  example,  when  there  is  marked 
anpeinia  in  a  woman  who  has  had  acute  rheumatism,  or  when 
a  murmur  is  present,  without  anaamia  adequate  to  account 
for  it,  in  a  patient  who  is  not  known  to  have  suffered  from 
rheumatism.  In  such  doubtful  cases,  the  character  of  the 
murmur  may  afford  useful  information.  If  the  murmur  is 
soft  and  blowing,  and  a  murmur  is  heard  not  only  at  the 
apex,  but  at  the  pulmonic  and  aortic  areas,  the  probability 
is  that  it  is  due  to  anasmia,  and  not  to  actual  valvular  change. 

Hsemic  murmurs  are  usually  soft  and  blowing  in 
character,  not  harsh  or  musical,  and  they  do  not  replace  or 
extinguish  the  first  sound.  Generally  speaking,  they  are 
not  conducted  to  the  axilla  or  heard  over  the  back,  and  are 
not  accompanied  by  much  displacement  of  the  apex  beat. 
While  this  is  the  rule,  I  have  known  several  cases  in  which 
it  was  departed  from,  the  apex  being  displaced,  and  the 
murmur  heard  towards  the  axilla  or  over  the  back. 


1 68  HEART  DISEASE. 

Furthermore,  it  is  the  hsemic  murmur  which  is  most 
frequently  late-systolic  in  time,  that  is,  it  follows  the  first 
sound  at  an  appreciable  interval  instead  of  commencing 
synchronously  with  it. 

These  indications,  together  with  the  history  of  the  case 
and  the  physical  signs  present,  will  as  a  rule  be  sufficient  to 
clear  up  the  diagnosis  in  doubtful  cases. 

Regurgitation  in  Acute  Febrile  Diseases. — Eegurgitation 
of  similar  character  resulting  from  acute  disease  lasts  for 
a  short  time  only,  and  is  chiefly  interesting  from  the  fact 
that  it  is  not  uncommon  after  acute  rheumatism,  the  great 
cause  of  true  valvular  lesions.  It  is  often  impossible 
to  say  whether  a  soft  mitral  murmur  heard  towards  the 
close  of  an  attack  of  rheumatic  fever,  indicates  the  begin- 
ning of  actual  disease,  or  is  the  result  of  temporary 
functional  imperfection.  If  it  occurs  after  the  commence- 
ment of  systole,  and  especially  if  a  pulmonic  systolic 
murmur  is  also  present,  it  may  be  that  the  regurgitation 
is  due  to  dilatation  from  anasmia  or  loss  of  tone  of  the 
muscular  fibres,  the  result  of  myocarditis  ;  but  time  alone 
will  decide  with  certainty. 

Chorea. — The  mitral  murmur  associated  with  chorea 
frequently  persists  after  the  chorea  is  cured,  and  may  be 
the  result  of  endocarditis  which  has  damaged  the  valves 
during  acute  or  sub-acute  rheumatism,  which  is  so  frequently 
an  antecedent  or  accompaniment  of  chorea.  It  may,  how- 
ever, be  due  to  temporary  dilatation  of  the  heart,  and  dis- 
appear as  the  chorea  subsides  and  the  patient  improves  in 
general  health. 

The  cases  considered  constitute  the  mitral  incompetence 
of  early  life.  But  the  mitral  incompetence  may  be  estab- 
lished during  the  decline  of  life,  from  other  causes,  and  this 
class  of  cases  must  now  be  considered. 

The  Mitral  Regurgitation  of  Middle  and  Old  Age. — 
It    is    astonishing    how  frequently  this   is   met   with,  and 


MITRAL  INCOMPETENCE.  169 

how  imperceptibly  it  is  established.  In  some  cases  there 
is  no  obvious  organic  valvular,  or  structural  alteration ; 
commonly,  however,  there  is  considerable  dilatation  of  the 
auriculo-ventricular  opening,  and  no  definite  diagnosis  can 
be  made  between  this  condition  and  degenerative  changes, 
such  as  thickening  and  calcification,  slowly  taking  place 
in  the  valves. 

Mitral  Incompetence  and  High  Arterial  Tension— The 
mitral  orifice  may  be  greatly  stretched  so  as  to  admit 
three  or  four  fingers.  Sometimes,  from  the  condition 
of  rigor  mortis  in  the  muscle,  the  valves  seem  to  be 
apparently  capable  of  closing  it  more  or  less  perfectly 
when  tested  by  water  after  death,  though  during  life  re- 
gurgitation was  permitted  as  a  result  of  imperfect  co- 
aptation. Dilatation  of  the  ventricle  and  stretching  of  the 
auriculo-ventricular  opening  usually  take  place  together, 
but  by  no  means  to  a  corresponding  extent ;  either  orifice 
or  ventricle  may  be  disproportionately  enlarged.  The 
regurgitation  may  be  said  to  be  only  an  incident  of 
dilatation.  Undue  arterial  tension  will  have  a  most  im- 
portant place  among  its  causes,  and  I  have  watched  in  many 
cases  the  gradual  supervention  of  a  murmur  upon  sounds 
which  have  had  the  loud  and  sharp  character  produced 
by  excessive  peripheral  resistance  ;  but  I  have  also  found 
a  mitral  murmur  when  there  has  been  no  arterial  tension, 
the  pulse  being  large,  soft,  short,  and  compressible.  In 
chronic  disease  of  the  kidneys,  which  can  scarcely  escape 
mention  when  the  effects  upon  the  heart  of  protracted  high 
tension  in  the  arteries  are  under  consideration,  mitral 
regurgitation  is  less  frequent  than  might  perhaps  have 
been  expected,  and  when  it  occurs,  there  is  usually  actual 
lesion  of  the  valves.  This  is  probably  due  to  the  fact  that 
the  hypertrophy,  which  is  associated  with  the  dilatational 
and  is  usually  the  predominant  change,  renders  the  ventri- 
cular systole  efficient  in  constricting  the  orifice. 


170  heart  disease. 

Teeatment. 

Mitral  incompetence  is  met  with  in  such  varied  degree 
and  has  such  varied  causation,  that  it  is  necessary  in 
discussing  the  treatment  to  differentiate  between  the  most 
important  varieties. 

1.  When  there  is  no  valvular  lesion,  and  the  regurgita- 
tion is  due  to  imperfect  systolic  narrowing  of  the  orifice  as 
in  anaemia,  and  occasionally  after  acute  disease,  the  principal 
treatment  will  be  that  of  the  condition  which  has  given  rise 
to  the  atony  of  the  cardiac  muscle.  When  the  heart  is  dilated 
after  acute  disease,  a  period  of  absolute  rest  may  occasionally 
be  necessary.  Violent  or  sustained  exertion  in  such  cases 
and  in  anaemia,  must  be  avoided,  as  acute  dilatation  may  be 
produced,  or  a  pre-existing  dilatation  may  be  increased  by  a 
comparatively  slight  cause.  Gentle  regular  exercise  will  be 
of  great  importance,  and  may  be  gradually  increased  in 
duration  and  vigour,  as  the  heart  regains  its  tone. 

A  daily  period  of  repose  in  the  recumbent  position 
should  be  enjoined,  and  a  complete  rest  for  a  certain  time 
before  and  after  meals  should  be  insisted  on. 

Climate  has  an  extraordinary  influence  in  this  condition 
of  heart,  and  the  GErtel  system  of  graduated  exercise  at  a 
moderate  elevation  is  often  of  great  service. 

Iron,  quinine  and  strychnine  may  be  given  for  the 
anaemia  and  general  weakness,  and  small  doses  of  digitalis 
will  often  make  a  great  difference  in  the  results  obtained. 

The  systolic  apex  murmur  may  be  confidently  expected 
to  disappear  in  time,  as  a  result  of  suitable  treatment. 

2.  In  the  case  of  a  systolic  apex  murmur  with  extremely 
little  regurgitation,  common  after  middle  age,  when  not 
due  to  dilatation  of  the  left  ventricle,  little  treatment  is 
required. 

In  most  cases,  instead  of  restriction  in  exercise  being 
necessary,  regular  exercise  will  have  to  be  ordered,  and  a 


MITRAL  INCOMPETENCE.  171 

sedentary,  self-indulgent  mode  of  life  modified,  as  these 
patients  often  plead  a  weak  heart  as  an  excuse  for  avoiding 
fresh  air  and  exercise,  which  they  dislike. 

When  the  incompetence  is  real,  and  has  required 
compensatory  changes  to  neutralize  its  effects,  it  is  still 
desirable  that  the  patient  should  take  regular  exercise,  the 
duration  and  vigour  of  which  must  be  determined  by  his 
strength  and  breath.  So  long  as  respiratory  distress  is  not 
induced,  outdoor  exercise  will  do  good  and  not  harm. 
Standing  about  indoors  is  much  more  likely  to  be 
injurious. 

The  one  contingency  to  be  specially  guarded  against 
is  bronchitis,  or  any  acute  affection  of  the  lungs.  The  pul- 
monary circulation  is  already  carried  on  under  difficulties, 
and  superadded  obstruction  may  intercept  the  compensatory 
high  pressure  maintained  in  the  left  auricle  by  the  right 
ventricle ;  the  result  being  that  there  is  less  opposition  to 
the  mitral  regurgitant  stream,  the  left  ventricle  is  imper- 
fectly filled,  and  the  systemic  blood  supply  is  impaired  : 
further,  the  right  ventricle,  unable  to  contend  with  the 
double  obstacle  to  the  transmission  of  blood  through  the 
lungs,  becomes  over-distended  and  crippled,  so  that  tricuspid 
regurgitation  and  venous  stasis  result.  The  dreaded  ulterior 
effects  of  mitral  regurgitation  are  thus  anticipated,  and, 
besides  this,  recovery  from  the  bronchitis  is  retarded  by 
the  congestion  in  the  pulmonary  capillaries. 

High  Arterial  Tension. — Precautions  must  also  be  taken 
against  high  arterial  tension,  which  may  be  due  to  renal 
disease  or  gout,  or  may  be  produced  by  too  nitrogenized 
a  system  of  diet,  or  by  habitual  consumption  of  beer  or 
strong  wines,  or  by  constipation.  With  high  arterial 
tension  there  will  be  increase  in  peripheral  resistance,  and 
thus  increase  in  the  amount  and  force  of  the  mitral  reflux, 
causing  an  additional  continuous  strain  on  the  compensatory 
mechanism.     Suitable  dieting   and  the   habitual  use   of    a 


172  HEART  DISEASE. 

mild  mercurial  purge  once  or  twice  a  week,  will  tend  to 
keep  down  high  arterial  tension  when  it  is  present. 

3.  When  serious  symptoms  set  in,  and  especially  if  any 
exciting  cause  can  be  traced,  there  is  more  chance  of  making 
head  against  them,  and  of  improvement  under  treatment, 
than  in  other  forms  of  valvular  disease.  The  result  of  mitral 
regurgitation  is  always  backward  pressure,  taking  effect 
first  on  the  lungs,  then  on  the  right  ventricle,  and  finally 
giving  rise  to  obstruction  to  the  systemic  venous  return, 
when  the  right  ventricle  breaks  down.  Tricuspid  regurgi- 
tation does  not  appear  to  add  appreciably  to  the  obstruction 
in  the  great  veins,  and,  indeed,  is  thought  by  some  to 
prevent  paralysis  of  the  right  ventricle  from  over-dis- 
tension. The  two  problems  in  the  treatment  are  the 
relief  of  the  venous  stagnation  and  the  strengthening  and 
restoration  of  tone  and  vigour  to  the  right  ventricle,  so 
that  it  can  again  perform  its  work  efficiently.  There  is 
no  constricting  barrier  opposing  a  fixed  mechanical  obstruc- 
tion to  the  blood  current  as  in  mitral  stenosis  ;  the  task 
is  therefore  easier. 

Fur  the  Relief  of  the  Venous  Obstruction,  purgatives,  of 
which  mercury  in  some  form  is  a  constituent,  will  usually 
be  sufficient,  repeated  according  to  their  effect,  and  accord- 
ing to  the  condition  and  strength  of  the  patient  every 
second  or  third  day.  The  application  of  leeches  over  the 
liver,  if  it  is  enlarged  and  tender,  will  often  be  of  great 
service,  and  almost  invariably  affords  relief.  Dry  cupping 
may  be  useful.  Yenesection  is  not  often  absolutely  required, 
though  probably  it  might  more  frequently  be  resorted  to 
with  advantage  than  is  the  case. 

Concurrently  digitalis  should  be  given,  and  it  is  in  the 
treatment  of  dropsy  and  advanced  conditions  of  mitral 
incompetence,  that  it  may  be  administered  with  the  greatest 
confidence  and  least  apprehension  of  its  so-called  cumulative 
effects.     It  increases,  it  is  true,  the  peripheral  resistance, 


MITRAL   INCOMPETENCE.  i73 

but  as  long  as  the  structures  of  the  heart  are  sound,  it 
appears  to  increase  the  vigour  of  its  contraction  in  greater 
proportion;  this  is  especially  the  case  with  the  right 
ventricle,  and  the  improvement  in  the  transit  of  blood 
through  the  lungs  is  perhaps  the  most  important  element 
in  its  beneficial  results.  It  may  be  given  with  satisfactory 
results  for  any  length  of  time,  as  there  is  no  barrier  in  the 
shape  of  a  stenosed  orifice,  against  which  the  increased 
energy  expended  by  the  heart  will  be  exhausted :  the  only 
reason  for  discontinuing  it  will  be  nausea  or  loss  of  appetite, 
to  which  it  sometimes  gives  rise,  or  marked  diminution  in 
the  amount  of  urine  excreted. 


CHAPTER   XII. 
MITEAL  STENOSIS. 

ETIOLOGY — PREDOMINANCE  IN  THE  FEMALE  SEX — MOEBID 
ANATOMY — PHYSIOLOGY  OP  THE  CHANGES  IN  THE 
HEART  —  BROWN  INDURATION  OP  LUNGS  —  NUTMEG 
LIVER  —  THE  PHYSICAL  SIGNS  —  THE  PULSE  —  THE 
CHANGES  IN  THE  HEART — THE  CARDIAC  MURMURS — 
THREE  STAGES  IN  THE  PROGRESS  OP  THE  DISEASE  AS 
DEFINED  BY  AUSCULTATORY  SIGNS — THE  CHARACTER- 
ISTICS OF  THESE  THREE  STAGES— SYMPTOMS— DIAGNOSIS 
—  PROGNOSIS  —TREATMENT. 

Constriction  of  the  mitral  orifice  is  on  many  grounds  the 
most  interesting  of  the  valvular  affections  of  the  heart. 
It  is  a  common,  and  at  the  same  time  a  serious  form  of 
valvular  disease,  and  its  clinical  history  presents  peculi- 
arities, some  of  which  have  long  been  recognized,  while 
others  have  not  received  adequate  notice.  It  was  the  last 
of  the  valvular  diseases  to  be  associated  with  distinctive 
physical  signs,  and  to  Gairdner  the  credit  of  this  discovery 
is  due.  It  also  presents  greater  difficulties  in  diagnosis 
than  any  other  of  the  valvular  affections. 

Etiology. 

Acute  endocarditis  is  the  commonest  cause  of  mitral 
stenosis,  but  a  certain  interval  must  elapse  before  con- 
striction of  the  mitral  orifice  results,  as  this  is  mainlv  due 


MITRAL  STENOSIS.  175 

to  cicatricial  contraction  of  the  fibrous  tissue  formed  in  the 
process  of  repair  of  the  damaged  valves  after  inflammation. 
A  remarkable  fact  is  the  relative  frequency  of  its  occur- 
rence   in   women,  whether    the    basis    of  the    estimate   is 
post-mortem  or  clinical.     Of  fifty-three  patients  dying  in 
St.  Mary's  Hospital  and  examined  after  death,  thirty-eight 
were   females   and   only   fifteen   males  —  seventy-two    and 
twenty-eight  per  cent,  respectively.      Of  eighty-one  cases 
collected  by  Hayden  fifty-four  were  females  and  twenty- 
seven  males — 66-6  and  33*3  per  cent.     Dyce  Duckworth,  in 
eighty  cases,   found   no  fewer   than   sixty-three    women — 
78*75  per  cent.     It  cannot  be   said   that   any  satisfactory 
explanation  of  this  great  disproportion  of  women  affected 
by  mitral  stenosis  has  been  given.    It  is  true  that  rheumatism 
is  more  common  in  girls  than  in  boys,  but  were  this  the 
only  reason,  there  ought  only  to  be  a  general  predominance 
of  valvular  disease  in  women,  and  not  of  this  particular  con- 
dition.    Possibly  the  greater  liability  of  girls  to  ansemia  at 
the  period  of  puberty  may  have  some  bearing  on  the  greater 
incidence  of  mitral  stenosis  in  the  female  sex,  especially 
when  it  is  borne  in  mind  that  ansemia  is  frequently  attended 
with  augmented  arterial  tension  which,  by  increasing  the 
stress  on  the  mitral  valves,  is  a  cause  of  insidious  damage. 
These  two   factors  may   tend  to   keep   going  the    chronic 
inflammatory  process,  which  results  in  adhesion  of  the  cusps 
of  the  mitral  valve,  and  in  further  constriction  of  its  orifice 
by  cicatricial  contraction  of  the  fibrous  tissue  thrown  out 
around  it. 

Morbid  Anatomy. 

The  Heart. — As  a  rule  the  heart  is  not  very  large.  Weights 
of  ten  and  twelve  ounces  are  common,  and  fourteen  or  fifteen 
will  represent  about  the  average.  The  left  ventricle  is 
usually  not  increased  in  size,  the  left  auricle  is  dilated 
and  hypertrophied,  and  the  right  ventricle  much  enlarged 


176  HEART  DISEASE. 

and  its  walls  greatly  thickened.  The  left  ventricle,  how- 
ever, may  be  enlarged  and  its  walls  thickened  if  mitral 
incompetence  preceded  the  mitral  stenosis,  and  there  may 
therefore  be  great  differences  in  the  weight  of  the  heart 
and  dimensions  of  its  cavities  in  different  cases. 

The  Mitral  Orifice. — The  condition  of  the  mitral  orifice 
may  vary  greatly,  and  an  extreme  degree  of  stenosis  does 
not  seem  to  be  incompatible  with  life.  The  orifice  may  be 
so  constricted  that  it  will  scarcely  admit  a  penholder,  and 
very  commonly  it  will  only  admit  the  tip  of  the  little  finger. 
To  such  conditions  the  term  "  button-hole  "  has  been  applied, 
but  it  is  scarcely  applicable,  as  the  margins  of  the  orifice 
are  usually  rigid  and  unyielding.  In  other  cases  the  aperture 
may  be  funnel-shaped.  Frequently  there  is  no  trace  of  the 
mitral  valves  remaining  as  such,  as  they  are  adherent  at  the 
margins,  contracted  down  to  form  a  rough  irregular  lining 
to  what  is  left  of  the  original  mitral  orifice. 

The  characteristic  physiological  effect  of  the  lesion  upon 
the  heart  is  dilatation  of  the  left  auricle  with  more  or 
less  thickening  of  its  wall,  and  great  hypertrophy  with 
some  dilatation  of  the  right  ventricle.  The  left  ventricle 
is  not  correspondingly  enlarged,  and  may  retain  its  normal 
size,  while  the  right  ventricle,  by  its  growth,  may  displace 
it  backwards,  so  that  no  part  of  it  appears  on  the  anterior 
aspect  of  the  heart,  and  its  apex  is  no  longer  in  contact 
with  the  chest  wall. 

When  the  mitral  orifice  is  narrowed,  it  is  the  left  auricle 
and  right  ventricle  only  which  are  called  upon  to  exert 
increased  force,  since  there  is  no  obvious  cause  of  increased 
resistance  in  the  systemic  circulation.  The  same  may  be 
said  when  the  valvular  lesion  is  mitral  incompetence  with 
regurgitation;  but  here  another  element  of  change  comes 
in,  which  makes  a  difference  between  obstruction  and 
incompetence.  The  high  pressure  in  the  pulmonary  veins 
and  left  auricle,  which  is  a  result  of  the  damming  back  of 


MITRAL   STENOSIS.  177 

the  blood  and  of  the  increased  force  of  the  right  ventricle, 
causes   a   forcible   inrush    into   the    left    ventricle    during 
diastole ;   and  this,  so  long  as  the  orifice    remains  of  the 
natural  size,  must  distend,  and  in  the  long  run  dilate  its 
cavity,   taking   effect,  as  it  does,   during   the   unresisting 
period  of  the  ventricular  rhythm.     But  an  increase  in  the 
capacity  of  the  cavity  multiplies  by  so   much   the   force 
required    to    expel    its    contents,    and    this    constitutes    a 
demand   for    hypertrophy.     We  have,  then,  as  a  result  of 
mitral  incompetence,  dilatation,  and  more  or  less  hyper- 
trophy of  the  left  ventricle ;  but  the  hypertrophy  here  is 
required  as   compensation  for  the   dilatation,  and   not  to 
overcome    any    direct    effect    of    the    impairment    of   the 
valvular  apparatus.     In  stenosis  of  the  mitral  orifice,  the 
pressure  which  thus  affects  the  left  ventricle  is  intercepted 
by  the  narrowed  orifice.     There  is  scarcely  time  for  it  to  be 
adequately  filled  during  diastole,  still  less  for  any  distending 
effect  to  be  produced.     We  see,  then,  how  it  is  that  the  left 
ventricle  usually  remains  of  normal  size  and  does  not  in- 
crease 'pari  passu  with  the  right.      Frequently,  however, 
the   left  ventricle  is    dilated  and  more    or  less  thickened, 
and  here  our  reasoning  appears  to  be  at  fault.     But  the 
difficulty  disappears  on  reflection.     Not  uncommonly  the 
change  in  the  valves,  which  eventually  glues  them  together 
and  narrows  the  orifice,  only  interferes  at  first  with  their 
apposition  and  permits  of  regurgitation,  which  may,  indeed, 
be  for  a  long  time  the  predominant  result ;  and,  in  point 
of  fact,  incompetence  often  precedes  the  establishment  of 
obstruction.     We  have  here  abundant  cause  for  differences 
in  the  condition  of  the  walls  and  cavities  of  the  heart  found 
after  death,  and,  it  must  be  added,  for  variations  in  the 
clinical  history,   and   especially  for  diversity  of   physical 
signs. 

The    Lungs.      Passive    Hyperemia.      Brown    Induration. 
(Edema. — As    a    result    of   prolonged    obstruction    to    the 

N 


178  HEART  DISEASE. 

flow  of  blood  from  the  lungs  to  the  left  auricle  in  mitral 
incompetence  and  stenosis,  there  is  passive  hypereemia  of 
the  lungs.  To  a  certain  extent  this  is  overcome  by  the 
increased  driving  power  of  the  hypertrophied  right  ventricle. 
But  the  high  pressure  thus  induced  in  the  pulmonary  circu- 
lation gives  rise  to  certain  pathological  changes  in  the 
lungs. 

The  capillaries  in  the  walls  of  the  alveoli  are  over- 
distended,  and  become  tortuous,  projecting  into  the  alveoli. 
Exudation  of  white  and  red  blood  cells  into  the  alveoli 
takes  place  and  occasionally  capillaries  rupture,  giving  rise 
to  slight  haemoptysis,  which  is  frequently  met  with  in 
mitral  stenosis  even  in  the  early  stages.  Some  of  the 
extravasated  blood  may  be  thus  expectorated,  some  is  taken 
up  by  the  alveolar  cells  and  lymphatics,  and  the  walls  and 
lymphatics  of  the  alveoli  are  often  loaded  with  granules  of 
pigment  derived  from  the  disentegrated  haemoglobin. 

As  a  result  of  the  irritation,  proliferative  changes  take 
place  in  the  alveolar  walls,  which  become  thickened,  lose 
their  elasticity,  and  tend  to  shrink  and  collapse,  so  that 
the  surface  available  for  aeration  of  the  blood  is  seriously 
impaired  and  diminished.  It  may  be  still  further  diminished 
by  patches  of  catarrhal  inflammation. 

This  condition  of  lung,  from  its  tough,  inelastic  feel, 
resulting  from  the  diffuse  fibrosis,  and  the  brownish  colour 
due  to  the  deposit  of  blood  pigment,  is  known  as  "  Brown 
Induration." 

As  will  be  readily  understood,  this  condition  is  most 
likely  to  arise  in  cases  of  mitral  stenosis,  where  the  hyper- 
trophied right  ventricle  has  to  keep  up  sufficient  pressure 
in  the  pulmonary  circulation  to  force  the  blood  through  the 
narrowed  mitral  orifice  which  constitutes,  in  severe  cases, 
an  almost  impenetrable  barrier  to  the  on-flow  of  the  blood. 
In  mitral  incompetence  the  back  pressure  is  more  variable 
and  is  usually  not  so  severe,  and  we  are  more  likely  to 


MITRAL  STENOSIS.  179 

meet  with,  a  condition  of  congestion  varying  in  degree 
from  time  to  time.  When  the  stagnation  of  the  circulation 
in  the  lungs  becomes  more  intense,  oedema  of  the  bases 
of  the  lungs  may  supervene,  the  alveoli  becoming  filled 
with  serum  exuded  from  the  congested  vessels. 

Infarction. — In  the  later  and  final  stages  of  mitral 
stenosis,  or  of  mitral  stenosis  and  incompetence  combined, 
infarction  of  the  lungs  is  very  liable  to  occur. 

As  the  lung  is  freely  supplied  with  blood  vessels, 
infarction  does  not  occur  from  embolism  of  a  small  artery 
in  a  normal  lung,  as  is  the  case  in  the  spleen  or  kidney, 
since  collateral  circulation  is  readily  established.  This  has 
been  proved  experimentally  by  Welch  in  dogs,  and  has  also 
been  verified  at  post-mortems  by  the  finding  of  occluded 
vessels  without  any  resulting  infarct.  When,  however, 
there  is  extreme  congestion  of  the  lungs  and  the  circulation 
is  obstructed  and  stagnant,  embolism  will  give  rise  to  an 
infarct,  as  collateral  circulation  cannot  be  established.  It 
has  been  supposed  that,  in  mitral  stenosis,  embolism 
occurs  from  clots  forming  in  the  right  auricle  during  life 
and  portions  becoming  detached  and  carried  to  the  lungs. 
I  have  never  seen  any  foundation  in  fact  for  this  theory, 
and  it  is  scarcely  conceivable  that  clotting  should  take 
place  in  the  heart  during  life  if  its  walls  are  healthy. 

It  is  probable  that  the  infarction  which  is  common  in 
the  later  stages  of  mitral  stenosis  is  the  result  of  thrombosis. 
There  is  intense  congestion  and  stagnation  in  the  capillaries 
and  small  arteries,  and  the  limit  at  which  the  circulation 
can  be  maintained  is  reached  at  last.  Stasis  and  gradual 
thrombosis  occur  in  one  or  more  of  the  smaller  arteries,  and 
the  result  is  the  same  as  in  embolism.  The  blood-supply  to 
the  area  supplied  by  the  artery  is  cut  off,  and  temporarily  it 
becomes  anaemic.  But  blood  soon  flows  from  the  adjoining 
capillaries  into  the  empty  vessels,  the  walls  of  which,  deprived 
of  their  nutrition,   give   way  or  allow  the  blood  to 


I  So  HEART  DISEASE. 

through  them  into  the  alveoli,  by  actual  rhexis,  or 
diapedesis,  so  that  we  get  a  large  hsemorrhagic  infarct. 
The  name  "  pulmonary  apoplexy  "  has  been  applied  by 
some  authors  to  this  condition,  but  it  scarcely  seems  a 
suitable  term,  as  it  is  not  the  rupture  of  a  vessel  which 
is  primarily  responsible  for  the  lesion. 

The  infarcted  areas  are  usually  of  considerable  size,  and 
more  or  less  wedge-shaped  with  their  base  at  the  pleura,  and 
may  measure  from  half-inch  to  three  or  four  inches  across 
at  their  widest  part.  They  are  often  multiple,  and  are 
usually  among  the  incidents  of  the  closing  scenes  in  the 
disease. 

The  Liver. — As  the  pressure  in  the  pulmonary  circulation 
is  greatly  increased,  it  stands  to  reason  that  the  pressure  in 
the  right  ventricle  in  systole  must  be  raised  in  proportion.  If 
the  ventricle  is  unequal  to  the  task  of  maintaining  the  high- 
pressure  circulation  it  may  dilate,  giving  rise  to  incom- 
petence of  the  tricuspid  valve,  or  may  inconipletety  empty 
itself  during  systole,  which  tends,  in  either  case,  to  dam  back 
the  blood  in  the  right  auricle.  This  will  cause  obstruction 
to  the  return  of  blood  to  the  auricle  from  the  great  veins. 
The  blood  in  the  inferior  vena  cava,  and  consequently  that  in 
the  hepatic  veins  being  dammed  back,  will  give  rise  to  conges- 
tion of  the  liver.  The  intra-lobular  veins  and  the  capillaries 
entering  them  in  the  centre  of  the  liver  lobules,  become 
distended  and  engorged  with  blood.  The  pressure  on  the 
adjoining  cells  in  the  centre  of  the  lobule,  and  impairment 
of  their  nutrition  results  in  atrophy  of  these  cells,  while 
fatty  degeneration  is  prone  to  occur  in  the  cells  in  the 
periphery  of  the  lobule.  The  liver  is  engorged  with  blood, 
and  greatly  increased  in  size ;  and  on  making  a  section  of 
the  liver  post-mortem,  we  see,  naked  eye,  the  congested 
capillaries  and  vein  in  the  centre  of  the  lobules  as  small 
red  areas  surrounded  by  yellowish,  opaque  rings  of  cells  in 
a  state  of  fatty  degeneration,  a  condition  which  is  known  as 


MITRAL   STENOSIS.  1S1 

a  "Nutmeg  Liver  "  from  its  appearance.  A  certain  amount 
of  secondary  fibrosis  may  occur  in  chronic  cases  of  long 
duration,  especially  in  mitral  stenosis. 

The  Kidneys.— As  a  result  of  chronic  congestion  pre- 
valent throughout  the  venous  system,  the  kidneys  become 
congested.  The  stellate  veins  are  especially  prominent, 
and  the  capillaries  of  the  malpighian  tufts  are  swollen  and 
distended  with  blood.  The  organ  is  often  of  a  bluish  colour, 
when  seen  at  the  post-mortem,  and  is  hard,  rounded,  and  very 
firm  on  section  from  secondary  diffuse  fibrosis  chiefly  marked 
round  the  congested  vessels.     This  condition  is  known  as 

"  Cyanotic  Induration." 

* 

Physical  Signs. 

The  Pulse. — The  pulse  of  mitral  stenosis  is  interesting. 
It  is  almost  always  regular  until  the  heart  is  obviously 
failing,  unless  the  obstruction  be  complicated  by  regurgi- 
tation or  by  valvular  affection  of  the  right  side  of  the 
heart. 

The  artery  at  the  wrist  is  small,  and  is  full  between  the 
beats,  presenting  the  characters  of  moderately  high  tension 
— that  is,  it  can  be  rolled  under  the  finger  and  is  not  very 
easily  compressed.  In  my  experience  this  modified  high 
tension  pulse  is  almost  constant,  and  it  points  to  resistance 
in  the  capillaries ;  but  the  cause  of  such  resistance  is  not 
readily  perceived.  It  may  be  due  to  contraction  of  the 
arterioles,  either  reflex  or  by  direct  stimulation,  consequent 
on  the  blood  being  charged  with  impurities  from  im- 
perfect elimination,  or  possibly  be  caused  by  backward 
pressure  in  the  veins,  which  makes  itself  felt  through  the 
capillary  network.  More  probably,  however,  it  is  simply 
an  effect  of  the  contracting  down  of  the  entire  arterial 
system  owing  to  the  diminished  supply  of  blood  from  the 
imperfectly  filled  left  ventricle. 


iS2  HEART  DISEASE. 

When  irregularity  comes  on,  it  is  usually  at  first  in- 
equality in  the  force  of  the  beats,  without  marked  disturb- 
ance of  the  rhythm.  Then  some  of  the  beats  of  the  heart 
fail  to  reach  the  wrist — no  doubt  from  inadequate  filling 
of  the  ventricle ;  the  action  of  the  heart  may  thus  continue 
to  be  regular  when  the  pulse  is  irregular.  In  some  rare 
instances,  there  is  only  one  beat  of  the  pulse  for  every  two 
beats  of  the  heart,  the  contraction  of  the  left  ventricle  at 
every  alternate  systole  being  inadequate  to  raise  the  aortic 
valves ;  and,  on  listening  to  the  heart,  there  will  be  no 
aortic  second  sound  with  the  alternate  systoles,  the  rhythm 
as  expressed  by  the  sounds  being  one — two — one,  one — two 
- — one,  with  an  accent  on  the  third  sound  heard.  The 
heart-beats  follow  each  other  in  couples,  and  the  accentuated 
first  sound,  unaccompanied  by  an  aortic  second  sound,  is 
mainly  produced  by  the  abrupt  contraction  of  the  right 
ventricle. 

The  Heart. — The  cardiac  sounds  and  murmurs  are  varied, 
and  sometimes  perplexing  ;  but  it  has  appeared  to  me  that 
they  afford  a  means  of  estimating  approximately  the  degree 
of  constriction  which  the  mitral  orifice  has  undergone.  The 
contraction  does  not  take  place  all  at  once,  but  increases  by 
slow  degrees  through  many  months  or  years,  and  it  is  to  be 
expected  that  corresponding  change  in  the  physical  signs 
will  accompany  this  change  of  mechanical  conditions.  The 
physical  signs  are  not  the  same  in  a  given  case  from 
beginning  to  end,  and  by  following  the  modifications  of 
the  sounds  and  murmurs  which  gradually  supervene,  1  have 
been  led  to  recognize  three  stages  of  the  disease. 

The  heart  is  not  usually  greatly  enlarged ;  the  apex  is 
displaced  to  the  left  and  sometimes  also  downwards,  but 
it  is  found,  as  a  rule,  not  far  from  the  normal  situation. 

The  dilatation  of  the  left  auricle  gives  rise  to  an 
extension  of  dulness  outwards,  along  the  fourth  and  third 
left    intercostal    spaces,   and    the   dilatation   of  the    right 


MITRAL   STENOSIS.  183 

auricle  causes  dulness  beyond  the  right  border  of  the 
sternum. 

The  apex  beat  is  not  well  defined,  and  in  advanced  cases 
a  sharp  and  distinct  shock  is  felt  on  palpation,  which  has 
not  the  deliberate  thrusting  character  of  hypertrophy,  but 
is  more  like  a  tap.  A  thrill,  presystolic  in  time,  may 
usually  be  felt  at  the  apex  or  just  internal  to  it.  The 
impulse  of  the  right  ventricle  is  powerful,  lifting  the  lower 
end  of  the  sternum  and  adjacent  costal  cartilages,  and 
making  itself  seen  and  felt  in  the  epigastrium. 

Changes  in  the  dimensions  of  the  heart,  however,  have 
not  the  same  direct  relation  to  the  degree  of  valvular 
mischief  in  mitral  stenosis  as  in  other  valvular  diseases, 
and  it  is  by  means  of  auscultatory  signs  that  the  division 
into  stages  is  effected. 

The  pathognomonic  sign  of  mitral  stenosis  is  usually 
given  as  a  presystolic  murmur  heard  over  a  limited  area  at 
and  to  the  inner  side  of  the  apex  beat,  between  it  and  the 
left  border  of  the  sternum.  It  is  not  a  smooth,  blowing 
murmur,  but  has  a  rough,  vibratory  character,  and  is  often 
accompanied  by  a  thrill  perceptible  to  the  hand  at  the  same 
spot.  A  further  distinctive  feature  is  the  way  in  which 
it  runs  up  to  and  suddenly  ends  in  the  first  sound,  which 
tends  to  become  short  and  sharp,  and  is  itself  highly 
characteristic. 

Sometimes  in  children  after  an  attack  of  pericarditis, 
possibly  as  a  result  of  pericardial  adhesions,  or  in  association 
with  a  mitral  systolic  murmur,  a  kind  of  rumbling  pre- 
systolic murmur  is  audible,  when  no  constriction  of  the 
mitral  orifice  exists.  This  murmur  has  not,  however,  the 
vibratory  character  of  the  true  murmur  of  mitral  stenosis  ; 
nor  does  it  terminate  abruptly  in  the  first  sound ;  nor 
is  the  first  sound  modified  in  the  manner  described  above. 
Reduplication  of  the  first  sound  should  not  be  mistaken 
for  a  presystolic  murmur. 


1 84  HEART  DISEASE. 

The  pulmonic  second  sound  is  accentuated,  as  a  result  of 
the  backward  pressure  in  the  pulmonary  circulation,  and 
very  frequently  there  is  reduplication  of  the  second  sound, 
from  want  of  synchronism  in  the  closure  of  the  pulmonic 
and  aortic  valves. 


Characteristics  of  the  Three  Stages  in  the  Progress 
of  the  Disease,  as  defined  by  Auscultatory  Signs. 

In  the  first  stage  a  second  sound,  as  well  as  a  presystolic 
murmur  and  first  sound,  will  be  audible  at  and  to  the 
left  of  the  apex.  It  is  the  persistence  of  the  second  sound 
at  the  apex  which  is  the  chief  distinctive  feature  of  this 
stage.    The  second  sound  may  be  reduplicated. 

Under  these  conditions  I  have  never  known  serious 
symptoms  to  arise  from  the  condition  of  the  heart,  and  I 
have  seen  illnesses  of  different  kinds,  even  serious  attacks 
of  bronchitis,  passed  through  without  the  intervention  of 
embarrassment  of  the  circulation.  It  is  very  rarely  that 
patients  are  admitted  into  hospital  presenting  simply  the 
signs  above  enumerated,  but  they  are  frequently  met  with 
in  out-patient  practice  and  in  consulting-rooms. 

The  Second  Stage.  — This  is  marked  by  the  disappearance 
of  the  second  sound  at  the  apex,  and  by  the  short,  sharp 
character  of  the  first  sound,  which  also  usually  becomes 
very  loud  ;  the  first  sound,  in  effect,  comes  to  resemble 
a  second  sound.  Mistakes  in  diagnosis  may  now  be  easily 
made.  In  mitral  stenosis,  at  this  stage,  and  in  mitral 
incompetence  there  is  alike  heard  at  the  apex  a  murmur 
followed  by  a  short,  sharp  sound  ;  but  in  the  former  the 
murmur  is  presystolic  in  time,  and  the  sound  is  the  modified 
first  sound,  while  in  the  latter  the  murmur  is  systolic  and 
the  sound  is  the  second  sound.  Very  slight  attention  would, 
in  most  cases,  suffice  to  prevent  any  confusion  between  the 
two,  but  an  apex  murmur  is  liable  to  be  set  down  as  the 


MITRAL   STENOSIS.  1S5 

familiar  systolic  murmur  of  regurgitation  without  further 
investigation,  and  thus  mitral  stenosis,  the  most  serious  of 
the  diseases  of  the  valves,  at  a  period,  too,  when  symptoms 
may  be  impending,  is  taken  for  incompetence,  which  is 
attended  with  less  danger  than  any  other  of  the  valvular 
affections.  To  bear  this  source  of  error  in  mind  is  to  avoid 
it ;  but  cases  are  sometimes  met  with  in  which,  from 
absence  of  cardiac  impulse  and  from  the  similarity  between 
the  sounds,  it  is  not  easy  to  follow  the  rhythm  of  the  heart 
and  time  the  murmurs  and  sounds.  Flexible  stethoscopes  are 
here  at  a  disadvantage  as  compared  with  the  rigid  wooden 
instrument,  which  communicates  to  the  ear  and  head,  not 
only  sound,  but  a  sense  of  shock  which  at  once  indicates 
the  moment  of  the  systole,  and  this  when  there  is  no 
impulse  perceptible  to  the  hand.  To  attempt  to  time  the 
first  sound  by  the  radial  pulse  is,  of  course,  fallacious.  The 
carotid  pulse  is  a  safer  guide,  but  it  is  not  always  easy  to 
co-ordinate  tactile  and  auditory  impressions. 

The  most  trustworthy  method  of  determining  the 
relation  of  sounds  to  the  cardiac  rhythm  is  to  find  a  spot  in 
the  region  of  the  base  where  the  first  and  second  sounds  are 
unmistakably  recognized,  and  then  from  this  point  to 
follow  the  sounds,  step  by  step,  toward  the  apex,  when  it 
will  be  found  which  of  them  it  is  that  disappears,  or  which 
maintains  some  distinguishing  peculiarity. 

The  presystolic  murmur  itself  usually  undergoes  a 
modification  in  this  stage.  As  commonly  heard,  it  occupies 
the  end  of  the  diastolic  interval,  running  up  to  the  first 
sound,  and  corresponding  therefore  with  the  auricular 
systole.  But  it  may  be  a  long  or  a  short  murmur,  and  may 
indeed  occupy  the  entire  diastolic  interval,  when  it  will 
correspond,  not  only  with  the  auricular  systole,  but  also 
with  the  active  diastolic  rebound  of  the  ventricle  from 
contraction ;  that  is,  the  murmur  is  produced  by  the 
current  of  blood  sucked  into  the  ventricle  as  it  dilates,  as 


1 86 


HEART  DISEASE. 


well  as  by  that  driven  into  it  by  the  systole  of  the  auricle. 
This  murmur,  occupying  the  whole  of  the  diastolic  interval, 
is  most  frequent  in  bad  cases.  But  it  may  further  be  cut 
in  two,  and,  instead  of  being  a  continuous  rumble  from  the 
second  sound  up  to  the  first,  may  subside  as  the  active 
dilatation  of  the  ventricle  ends,  and  before  the  auricular 
systole  begins ;  or  the  proper  presystolic  part  of  the 
murmur  may  be  lost  while  the  diastolic  part  remains 
audible,  so  that  the  only  murmur  heard  is  diastolic,  i.e. 
a  diastolic  mitral  murmur,  strictly  speaking.    These  varieties 


FIG.  19. — 1.  PRESYSTOLIC  MURMUR  CORRESPONDING  WITH  AURICULAR  SYSTOLE. 
2.  MURMUR  OCCUPYING  WHOLE  DIASTOLIC  INTERVAL.  3  MURMUR  DIVIDED 
INTO   DIASTOLIC   AND    PRESYSTOLIC   PORTIONS. 


of  murmur  may  be  represented  diagrammatically  as  shown 
in  Fig.  19. 

The  disappearance  of  the  second  sound  at  the  left  of  the 
apex,  which,  with  the  short,  sharp  character  of  the  first 
sound,  marks  the  second  stage  of  mitral  stenosis,  is  probably 
explained  by  the  following  considerations.  In  the  normal 
heart,  a  second  sound  is  always  audible  at  and  to  the  left 
of  the  apex;  and  repeated  careful  examinations  have  con- 
vinced me  that  it  is  the  aortic  second  sound  which  is  here 
heard,  and  not  the  pulmonic,  even  when  this  is  accentuated 
and  unduly  loud.  In  mitral  stenosis,  there  are  two  influences 
tending  to  prevent  the  aortic  second  sound  from  reaching 
the   surface    of  the   chest.     First,   the   left   ventricle,   not 


MITRAL  STENOSIS.  187 

undergoing  dilatation  and  hypertrophy,  while  the  right 
enlarges  greatly,  is  overlapped  by  the  latter,  which  usurps 
the  position  of  the  apex,  and  thus  the  left  ventricle  cannot 
conduct  the  aortic  sound  to  the  chest  wall.  Again,  the 
aortic  second  sound  will  be  weak,  because  the  diminished 
amount  of  blood  entering  the  ventricle,  in  consequence 
of  the  narrowed  mitral  orifice,  will  not  distend  the  aorta, 
and  will,  therefore,  fail  to  produce  a  powerful  recoil 
such  as  is  necessary  for  the  production  of  a  loud  second 
sound. 

The  modification  of  the  first  sound  in  mitral  stenosis  is 
remarkable,  and  in  searching  for  an  explanation  of  this,  one 
is  struck  by  the  analogy  of  the  sharp,  sudden,  and  tapping 
character  of  the  apex  beat  to  the  shortness  and  sharpness  of 
the  first  sound,  which  would  seem  to  imply  that  some 
common  cause  has  been  instrumental  in  the  production  of 
these  peculiarities  in  both  instances.  If  this  be  the  case, 
it  is  clear  that  the  ventricular  wall  must  be  one  of  the 
factors,  and  the  following  explanation  may  be  suggested. 
Owing  to  the  narrowing  of  the  mitral  orifice  there  is  not 
time  in  the  diastolic  interval  for  a  sufficient  amount  of 
blood  to  flow  into  the  left  ventricle  to  completely  fill  it. 
At  the  commencement  of  systole,  therefore,  the  ventricular 
cavity  is  not  fully  distended  with  blood,  so  that  the  muscular 
walls  at  the  first  moment  of  their  contraction  meet  with  no 
resistance ;  then,  closing  down  rapidly,  they  are  suddenly 
brought  up  and  made  tense  as  they  encounter  the  contained 
blood.  It  seems  plausible  that  this  sudden  tension  of  the 
muscular  walls  and  the  abbreviated  systole  of  the  left 
ventricle,  would  account  both  for  the  sharp  and  tapping 
apex  beat  and  for  the  short  first  sound. 

In  severe  palpitation  and  tachycardia  the  first  sound  is 
also  extremely  short  and  sharp,  and  probably  a  similar 
explanation  holds  good  here,  namely,  that  the  brief  diastolic 
interval  which  is  the  rule  in  such  cases  does  not  afford 


188  HEART  DISEASE. 

sufficient  time  for  the  complete  filling  and  distending  of 
the  ventricle  with  blood. 

The  third  stage  is  characterized  by  the  disappearance 
of  the  presystolic  murmur,  so  that,  the  second  sound  being 
already  lost,  the  only  sound  at  and  outside  the  apex  is 
the  short  sharp  first  sound  described.  This  is  not  unlike 
the  first  sound  heard  in  dilatation  with  thinning  of  the 
left  ventricle ;  but  the  absence  of  the  second  sound  to  the 
left  of  the  apex  constitutes  a  diagnostic  difference,  since 
this  is  distinct  in  dilatation. 

No  careful  observer  who  has  devoted  much  attention  to 
the  study  of  mitral  stenosis  has  failed  to  notice  that  the 
presystolic  murmur  is  sometimes  absent  in  cases  in  which 
an  advanced  stage  of  this  condition  is  met  with  after 
death.  The  principal  justification,  however,  for  taking  the 
disappearance  of  the  presystolic  murmur  as  a  distinct 
stage  in  the  clinical  history  of  mitral  stenosis  is  that, 
very  commonly  when  pulmonary  complications  set  in,  or 
other  serious  symptoms  arise,  the  presystolic  murmur  is 
lost,  and  that  it  again  becomes  audible  when  these  subside 
and  the  patient  improves. 

It  is  a  matter  of  repeated  and  familiar  experience  for 
cases  to  be  admitted  into  hospital  on  account  of  serious 
symptoms  with  only  the  short  sharp  first  sound  audible 
at  the  apex,  and  to  leave  after  recovery  with  a  presystolic 
murmur.  The  third  stage,  however,  is  not  necessarily 
attended  with  serious  symptoms,  though  this  is  the  rule. 

The  probable  cause  of  the  disappearance  of  the  murmur 
is  the  establishment  of  tricuspid  incompetence.  The  giving 
way  of  the  tricuspid  valve  and  the  occurrence  of  con- 
siderable reflux  into  the  right  auricle,  make  it  impossible 
for  the  right  ventricle  to  sustain  the  same  high  pressure 
in  the  pulmonary  circulation  and  left  auricle  as  was 
present  previously.  There  is  not,  therefore,  sufficient 
pressure  to  force  the  blood  through  the  mitral  orifice 
rapidly  enough  to  generate  a  murmur. 


MITRAL  STENOSIS. 


Symptoms. 


The  patient,  up  to  a  somewhat  advanced  stage,  has  not 
the  look  of  heart  disease,  is  neither  pallid,  nor  dusky, 
nor  anxious-looking,  but  often  has  a  bright  colour  and 
cheerful  expression.  There  is  some  breathlessness  on 
exertion,  but  not  infrequently,  up  to  the  moment  when, 
from  some  cause  or  other,  serious  symptoms  set  in,  he  or 
she  is  unconscious  of  serious  embarrassment  of  the  circula- 
tion, and  capable  of  ordinary  work.  The  capillaries  over  the 
cheek  bones  are  frequently  congested,  giving  a  ruddy  colour 
which  might  be  taken  for  a  sign  of  good  health,  were  it  not 
contradicted  by  the  dusky  cyanotic  tinge  of  the  lips.  The 
cyanosis  tends  to  become  more  marked  and  permanent  and 
the  dyspnoea  more  severe  in  the  later  stages,  from  the 
diminution  in  the  aerating  capacity  of  the  lungs,  which 
supervenes  as  their  condition  approximates  that  known  as 
"  Brown  Induration."  Such  patients  are  liable  to  cough 
and  haemoptysis  from  the  constant  high  pressure  in  the 
pulmonic  circulation.  In  the  early  stages  the  haemoptysis 
is  slight,  being  due  to  rupture  of  capillaries,  and  consists  of 
mucus  streaked  with  blood.  In  the  advanced  and  terminal 
stages  it  is  often  very  profuse  and  repeated,  being  due 
to  infarction.  Cough  is  often  a  troublesome  symptom, 
from  the  bronchial  catarrh  to  which  the  patient  is  especially 
liable.  Attacks  of  tachycardia  or  palpitation  are  common 
and  may  cause  great  distress.  Another  condition  more 
frequently  met  with  as  a  consequence  of  mitral  stenosis, 
than  in  other  valvular  affections,  is  great  enlargement  of 
the  liver,  with  true  pulsation  of  this  organ,  which  often 
feels  hard  and  firm  on  examination ;  it  is  not  uncommon 
to  find  fluid  in  the  peritoneal  cavity  before  there  is 
cedertia  of  the  feet  and  legs,  or  the  oedema  will  dis- 
appear with  rest  in  bed,  while  ascites  persists,  whereas 
dropsy,  in  cardiac  failure,  due  to  mitral  incompetence,  as 


igo  HEART  DISEASE. 

a  rule,  begins  in  the  connective  tissue  of  the  most  de- 
pendent parts,  and  ascites  is  not  common.  A  reference  to 
the  section  on  morbid  anatomy  will  make  clear  the  causa- 
tion of  most  of  the  symptoms. 

Diagnosis. 

In  the  first  stage,  where  the  vibratory  presystolic 
murmur  ending  in  the  short  sharp  first  sound,  and  the 
second  sound  are  present,  there  will  be  little  difficulty  in 
arriving  at  a  diagnosis.  The  short,  rumbling,  presystolic 
murmur  often  met  with  during  or  shortly  after  an  attack 
of  peri-  or  endo-carditis,  more  especially  in  children,  may, 
however,  lead  to  some  confusion.  This  murmur,  however, 
is  not  of  the  loud  vibratory  character  of  the  typical  pre- 
systolic murmur,  but  is  usually  short  and  rumbling ;  it  does 
not  indicate  the  presence  of  mitral  stenosis,  at  any  rate, 
in  the  sense  of  an  established  organic  lesion.  A  further 
distinctive  feature  in  diagnosis  will  be  the  absence  of  the 
typical  modification  of  the  first  sound,  which,  instead  of 
being  short  and  sharp,  will  be  dull,  low-pitched,  and 
possibly  reduplicated. 

In  the  second  stage,  when  the  second  sound  is  lost 
at  the  apex  and  only  the  presystolic  murmur  and  first 
sound  are  present,  these  may  possibly  be  taken  for  a 
systolic  murmur  and  second  sound  which  the  first  sound 
has  come  to  resemble  in  character ;  the  case  would  then  be 
mistaken  for  one  of  mitral  incompetence  in  which  the 
prognosis  is  much  less  serious.  Due  care  and  accurate 
timing  of  the  sounds  will  prevent  this.  Confusion  is, 
however,  liable  to  occur  when  mitral  regurgitation  is 
present  as  a  complication,  which  is  of  very  common 
occurrence.  It  is  then  possible  to  mistake  the  presystolic 
and  systolic  murmurs  together  for  a  prolonged  systolic 
murmur,   the   short   sharp   first  sound  being  taken  for  an 


MITRAL   STENOSIS. 


191 


accentuated  second  sound.  But  attention  to  the  character 
and  time  of  the  murmurs  will  obviate  such  a  mistake. 
The  systolic  murmur  of  mitral  regurgitation  is  blowing 
or  musical,  and  begins  with  an  accent,  whereas  the  pre- 
systolic murmur  is  vibratory  and  ends  with  an  accent. 
Accurate  observation  of  the  time  at  which  the  short  sharp 
sound  is  heard  will  also  prevent  the  mistake,  but  this 
will  not  perhaps  be  so  easily  distinguished  as  the  character 
of  the  murmurs. 

They  may  be  represented  diagrammatically  as  follows  :  — 


ilBu. 


fig.  20  (Dark  shading  =  presystolic  murmur ;  light  shading  =  systolic 
murmur). 

1.  ORDINARY  PRESYSTOLIC  WITH  SYSTOLIC  MURMUR.  2.  PRESYSTOLIC 
MURMUR  OCCUPYING  THE  WHOLE  OF  DIASTOLE,  WITH  SYSTOLIC  MURMUR. 
3.  DIASTOLIC  PORTION  ONLY  OP  PRESYSTOLIC  MURMUR  WITH  SYSTOLIC 
MURMUR. 

In  the  third  stage,  complicated  by  mitral  regurgitation, 
recognition  of  mitral  stenosis  will  often  present  great 
difficulties.  There  will  be  no  presystolic  murmur,  and 
only  a  first  sound  with  a  systolic  murmur  will  be  audible 
at  the  apex.  The  absence  of  the  second  sound  will  be  of 
great  value  in  identifying  the  stenosis.  If,  however,  the 
mitral  regurgitation  has  preceded  the  onset  of  stenosis,  it 
may  have  given  rise  to  a  degree  of  hypertrophy  and  dilata- 
tion of  the  left  ventricle,  such  that  the  apex-beat,  which 
comes  into  contact  with  the  chest  wall,  is  still  that  of 
the  left  ventricle  and  not  of  the  right,  so  that  the  aortic 
second  sound  is  still  conducted  to  the  chest  wall.     In  such 


192  HEART  DISEASE. 

cases  the  modification  of  the  first  sound  is  an  important 
aid  to  diagnosis;  regurgitation  tends  to  destroy  the  first 
sound,  stenosis  to  shorten  and  intensify  it,  so  that  the 
presence  of  a  short  sharp  first  sound  with  a  systolic  murmur, 
in  a  case  where  there  is  obviously  serious  cardiac  mischief, 
should  at  once  suggest  the  probability  of  the  presence  of 
mitral  stenosis. 

When,  however,  compensation  has  broken  down  in  a 
case  of  combined  stenosis  and  regurgitation,  extraordinary 
fluctuations  in  the  physical  signs  may  be  present ;  at  one 
time  a  systolic,  at  another  a  presystolic  murmur,  at  another 
time  both  may  be  heard,  or  perhaps  only  a  short  sharp 
sound  alternating  with  murmurs,  which  it  is  impossible 
to  time.  At  the  same  time  the  action  of  the  heart  will 
be  rapid  and  markedly  irregular.  In  such  cases  the  ex- 
traordinary fluctuations  must  themselves  give  the  chief 
clue  to  the  diagnosis,  though  it  will  be  impossible  to 
estimate  the  extent  of  either  lesion. 

It  would  appear  that  when  the  high  pressure  in  the 
left  auricle  is  well  sustained  it  generates  a  presystolic 
murmur,  and  prevents  regurgitation,  so  that  no  systolic 
murmur  is  generated,  and  there  is  no  reflux,  even  though 
the  typical  "  buttonhole  "  mitral  orifice  is  present,  in  which 
closure  of  the  orifice  is  absolutely  impossible,  as  no  valves 
in  fact  remain  as  such.  When,  on  the  other  hand,  the 
pressure  in  the  left  auricle  and  pulmonary  circulation  falls 
below  a  certain  point,  either  from  break-down  of  the  right 
ventricle  or  from  the  onset  of  tricuspid  regurgitation, 
mitral  reflux  takes  place  during  systole,  and  there  is  not 
sufficient  pressure  in  the  left  auricle  during  diastole  to 
generate  a  presystolic  murmur.  We  may  thus  explain 
these  extreme  and  confusing  varieties  in  the  physical 
signs  of  the  third  stage  of  mitral  obstruction  complicated 
by  regurgitation,  and  account  for  the  absence  of  a  systolic 
murmur  in  many  cases  where,  from  the  condition  of  the 


MITRAL  STENOSIS.  193 

mitral  orifice  post-mortem,  we  should  have  expected  mitral 
regurgitation  to  have  been  present  during  life. 

In  aortic  incompetence  a  presystolic  murmur  is  some- 
times present  in  addition  to  the  diastolic  murmur,  which 
does  not  necessarily  imply  the  existence  of  mitral  stenosis. 
The  probable  significance  of  this  murmur  and  the  explana- 
tion of  its  presence  have  already  been  discussed  in  the 
chapter  on  Aortic  Incompetence. 

Peognosis. 

Mitral  stenosis  stands  next  to  aortic  regurgitation 
among  valvular  affections  in  the  order  of  gravity.  The 
average  age  at  death,  as  deduced  from  53  cases  abstracted 
from  the  post-mortem  records  at  St.  Mary's  Hospital,  was 
found  to  be  33  for  males  and  37  or  38  for  females,  which 
is  higher  than  one  would  expect. 

A  suggestive  inquiry  is,  why  mitral  stenosis  should  be 
so  serious,  and  especially  why  it  should  be  attended  with 
greater  danger  to  life  than  mitral  incompetence.  One 
reason  is,  that  the  effects  of  obstruction  here  are  not  so 
easily  neutralized  as  are  the  effects  of  regurgitation.  The 
high  pressure  maintained  in  the  pulmonary  circulation  and 
in  the  left  auricle,  by  hypertrophy  of  the  right  ventricle, 
will  antagonize  incompetence  of  the  valve  in  two  ways — 
by  resisting  the  reflux  during  systole,  and  by  more  rapid 
filling  of  the  ventricle  during  diastole.  In  stenosis  this 
high  pressure  can  only  be  of  service  by  increasing  the 
rapidity  of  the  passage  of  blood  through  the  narrowed 
orifice  during  diastole ;  and,  as  diastole  only  lasts  for  a 
certain  time,  if  the  contraction  be  extreme,  the  ventricle 
cannot  be  properly  filled  before  the  systole  is  again  due. 
When  such  is  the  case,  the  compensation  is  inadequate. 
On  the  other  hand,  since  the  constriction  may  reach  a 
degree  which,  in  the  absence  of  experience,  would  seem 
quite  incompatible  with  life,  and  since  the  subjects  of  such 

o 


i94  HEART  DISEASE. 

extensive  change  must  have  lived  through  all  the  inter- 
mediate degrees,  it  can  scarcely  be  simply  that  obstruction, 
as  such,  is  specially  dangerous.  Probably  the  explanation 
of  the  greater  danger  of  obstruction,  as  compared  with 
regurgitation,  lies  in  the  fact  that,  when  once  adhesion 
between  the  flaps  of  the  valves  has  set  in,  it  tends  to  go 
on,  the  friction  and  strain  keeping  up  chronic  inflamma- 
tion, which  gives  rise  to  further  adhesion  of  the  valves  and 
contraction  of  the  orifice. 

When  mitral  stenosis  is  established  in  childhood  or 
early  adolescence,  the  prognosis  is  more  serious  than 
when  it  occurs  in  later  life.  This  is  partly  owing  to  the 
progressive  tendency  of  the  constriction  of  the  orifice, 
which  is  more  marked  in  early  life,  and  partly  to  the  fact 
that  the  stenosed  orifice  does  not  increase  in  size  while 
the  growth  of  the  heart  continues,  so  that  even  though  no 
further  actual  narrowing  takes  place,  the  relative  dispropor- 
tions between  the  mitral  orifice  and  the  cavities  of  the  heart 
will  increase  as  the  heart  attains  its  full  development. 

The  important  point  in  prognosis,  however,  is  the 
comparative  prospect  of  life  in  individual  cases,  and  it  is 
in  the  estimation  of  this  that  the  recognition  of  the 
different  stages  is  of  service.  The  extent  of  the  hyper- 
trophy and  dilatation  of  the  walls  and  cavities  of  the  heart 
does  not  afford  very  great  assistance,  as  we  have  seen  that 
mitral  stenosis  does  not  give  rise  to  any  marked  change 
in  the  left  ventricle ;  a  certain  amount  of  information, 
however,  as  to  the  amount  of  obstruction  may  be  gathered 
from  the  degree  of  hypertrophy  and  dilatation  of  the  right 
ventricle,  on  which  has  fallen  the  work  of  overcoming  the 
obstruction.  A  careful  study  of  the  sounds  and  murmurs 
will  give  more  precise  information,  so  that  the  three  stages 
in  the  disease,  as  described  above,  must  be  borne  in  mind 
in  attempting  to  form  a  prognosis.  So  long  as  the  second 
sound  is  heard  at  and  beyond  the  apex,  there  is  little  or 


MITRAL  STENOSIS.  195 

no  liability  to  the  occurrence  of  symptoms,  and  there  is 
no  immediate  danger.  It  must,  however,  be  borne  in  mind 
that,  owing  to  the  tendency  of  the  stenosis  to  increase,  the 
prognosis  as  to  prolonged  life  in  the  future  is  not  favour- 
able in  the  majority  of  cases. 

When  the  second  sound  is  lost  at  the  apex,  that  is, 
when  the  second  stage  is  reached,  there  may  still  be 
immunity  from  symptoms  under  ordinary  conditions  of 
life;  but  there  is  no  capacity  for  the  adjustment  of  the 
circulation  to  deviations  from  these,  so  that  any  imprudence 
or  slight  over-exertion,  or  even  mental  worry,  on  the  part 
of  the  patient  is  liable  to  bring  about  a  break-down  of 
compensation.  One  must  not,  therefore,  be  thrown  off 
one's  guard  by  absence  of  complaints,  or  by  the  apparent 
good  health  of  the  patient.  With  suitable  precautions 
and  care,  however,  the  condition  of  the  patient  may  remain 
the  same  for  years,  though  any  tendency  to  increasing 
shortness  of  breath  or  any  fresh  attack  of  rheumatism  will 
be  reasons  for  apprehension,  as  indicating  that  the  con- 
striction is  increasing. 

When  the  third  stage  is  reached  and  serious  syrnr)tonis, 
such  as  dyspncea,  dropsy,  pulmonary  infarction,  and  other 
effects  of  venous  congestion  and  over-distension  of  the 
right  side  of  the  heart,  are  present,  the  first  element  in 
the  mental  calculation  will  be  the  severity  of  the  symptoms. 
But  recoveries  are  witnessed  in  conditions  apparently  so 
desperate  that  if  it  is  the  first  time  the  patient  has  suffered 
from  a  similar  complete  break-down  of  compensation, 
the  case  must  not  be  pronounced  absolutely  hopeless.  The 
number  of  times  severe  symptoms  have  arisen  and  the 
readiness  with  which  they  have  been  provoked  become 
the  most  important  considerations.  If  the  patient  has  had 
similar  attacks  previously,  and  if  a  very  slight  cause  has 
been  sufficient  to  induce  them,  the  danger  is  very  great, 
and  the  chance  of  even  temporary  recovery  is  a  poor  one. 


196  heart  disease. 

Treatment. 

The  first  stage  of  mitral  stenosis  is  attended  with  few 
symptoms,  and  rarely  calls  for  treatment.  So  long  as  the 
narrowing  of  the  orifice  is  only  moderate,  compensation 
appears  to  be  easily  effected,  and  the  patient  suffers  little 
or  no  inconvenience.  The  fear  is  that  once  the  flaps  of 
the  valve  have  begun  to  adhere,  the  adhesion  will  extend 
and  gradually  narrow  the  fissure  between  them.  If  this 
could  be  prevented  by  any  means,  the  treatment  effecting 
it  would  be  of  extreme  value.  We  have  no  power,  how- 
ever, of  directly  influencing  the  process  of  adhesion,  and 
can  only  endeavour  to  obviate  causes  tending  to  keep  up 
or  excite  inflammation  of  the  valves.  Every  possible  pre- 
caution should  be  taken  against  rheumatism,  which  is 
extremely  prone  to  attack  the  damaged  valves ;  and  slight 
rheumatism,  which  might  be  neglected  in  a  sound  in- 
dividual, should  receive  attention  in  a  patient  suffering 
from  mitral  stenosis  of  however  small  degree.  Unduly 
high  pressure  in  the  arterial  circulation  will  react  on  the 
valves  by  giving  rise  to  high  intra-cardiac  pressure,  and 
stress  upon  them  will  tend  to  keep  up  or  revive  irritation. 
Over-eating  and  drinking,  again,  and  constipation,  giving 
rise  to  accumulation  of  impurities  in  the  blood,  will  have 
a  like  tendency.  Precautions  based  on  this  knowledge 
should  therefore  be  inculcated  upon  the  patient. 

Bronchitis  and  other  affections  of  the  lungs  will  increase 
the  resistance  in  the  pulmonary  circulation  and  the  strain  on 
the  right  ventricle,  and  should  be  specially  guarded  against. 

As  the  narrowing  of  the  orifice  progresses,  or  when 
the  affection  is  found  on  examination  to  have  reached 
the  second  stage,  and  when  symptoms  such  as  breathless- 
ness  and  cardiac  pain  or  oppression  or  weight  are  readily 
induced,  or  are  more  or  less  constantly  present,  or  when 
haemoptysis  has  occurred,  the  precautions  suggested  above 


MITRAL  STENOSIS.  197 

should  be  urged  more  emphatically.  Mercurial  purgatives 
will  then  be  of  service,  and  rest  in  the  recumbent  position, 
and,  if  necessary,  confinement  to  bed  for  a  time  should  be 
ordered.  Strychnia  and  iron,  with  nitroglycerine  or  nitrites 
and  stimulants,  may  be  prescribed,  but  digitalis  should 
not  be  given  unless  there  are  symptoms  of  right  ventricle 
failure,  and  not  then  until  after  free  purgation  ;  on  no 
account  should  it  be  given  for  a  long  period. 

The  rules  for  exercise  will  be  the  same  as  in  other 
forms  of  valvular  disease.  Sufferers  from  mitral  stenosis 
of  slight  or  moderate  degree  are  perhaps  more  liable  to 
do  themselves  harm  by  imprudent  exertion  than  the 
subjects  of  mitral  incompetence,  as  they  are  often  not 
checked  by  breathlessness,  but  persist  in  overtaxing  their 
strength  till  severe  pain  in  the  heart,  or  perhaps  an  attack 
of  haemoptysis  is  induced.  At  an  advanced  stage  of  the 
disease  exertion  may  prove  suddenly  fatal,  but  never  while 
the  patient  is  free  from  serious  symptoms ;  more  commonly 
it  is  by  overthrowing  the  compensatory  balance  already 
inclined  to  the  wrong  side,  and  so  aggravating  the  existing 
venous  stasis,  or  by  detaching  a  thrombus,  which  gives 
rise  to  embolism,  that  effort  or  excitement  proves  injurious 
and  ultimately  fatal.  Haemoptysis  is  rarely  considerable,  and 
seldom  requires  any  other  treatment  than  rest  and  aperients. 

When  from  neglect  of  precautions,  or  from  overtaxing 
of  strength  by  unavoidable  duties,  or  from  depressing 
emotions,  or  from  the  advance  of  the  disease,  decided 
symptoms  of  right-ventricle  failure  have  supervened,  such 
as  great  weakness,  cough,  dyspnoea,  with  evidences  of 
venous  stasis  in  swollen  jugulars  and  enlarged  liver,  and 
dropsy,  then  energetic  measures  will  be  required.  These 
will  be  mainly  such  as  will  relieve  the  venous  engorge- 
ment and  the  overloaded  right  ventricle  and  auricle, 
smart  purgation  by  calomel  or  blue  pill  and  colocynth, 
followed,  if  necessary,  by  salines. 


198  HEART  DISEASE. 

When  the  symptoms  are  very  urgent,  venesection  may 
be  of  striking  service,  and  in  certain  cases  there  is  no 
other  treatment  that  will  take  its  place  and  avail  to 
avert  a  speedy  fatal  termination. 

The  indications  will  be,  not  a  full  bounding  pulse,  but 
the  opposite — a  small,  weak,  irregular  pulse,  many  of  the 
beats  being  scarcely  perceptible ;  the  heart,  on  the  other 
hand,  more  especially  the  right  ventricle,  will  be  beating 
violently,  epigastric  pulsation  being  very  marked,  while 
the  apex  beat  is  scarcely  perceptible.  The  liver  will  be 
enlarged,  and  perhaps  pulsating,  and  the  jugulars  will  be 
full  and  pulsating.  The  contrast  between  the  powerful 
right  ventricle  impulse  and  the  small,  weak,  irregular  pulse 
is  very  striking,  and  is  one  of  the  most  important  indica- 
tions for  venesection.  The  sufferer  will  be  in  a  state  of 
dyspncea,  though  not  always  of  an  agonizing  kind,  and 
not  always  compelling  him  to  sit  up ;  the  face  may 
be  dusky  and  the  lips  blue,  but  it  may  also  be  pale  with 
a  red  patch  of  injected  capillaries  on  the  cheeks. 

The  narrowed  mitral  orifice  constitutes  a  fixed  obstacle, 
which  keeps  up  an  unremitting  backward  pressure  in  the 
pulmonary  circulation,  and  makes  it  difficult  or  impossible 
for  the  right  ventricle  to  overcome  the  paralyzing  over- 
distension to  which  it  is  subjected.  Venesection  lessens 
the  amount  of  blood  arriving  by  the  veins,  and  gives  the 
right  ventricle  a  chance  of  recovery,  so  that  it  can  again 
contract  down  more  or  less  efficiently  on  its  contents. 

Venesection  does  not,  however,  dispense  with  the 
necessity  for  relieving  the  portal  circulation  by  purgation. 
Stimulants  which  without  these  measures  afford  no  relief, 
and  may  indeed  do  harm,  will  then  be  of  the  greatest 
service,  and  digitalis  and  like  remedies  will  find  their 
opportunity. 

When  the  symptoms  are  less  urgent  or  venesection  is 
objected  to,  seven  or  eight  leeches  applied  over  the  liver 


MITRAL   STENOSIS.  199 

may  be  of  service,  and  in  hospital  patients,  where  rest  and 
care  and  proper  nourishment  make  such  an  enormous 
difference  in  the  influences  acting  on  the  patient,  leeches 
will  usually  be  sufficient. 

The  administration  of  digitalis  in  the  early  stages  of 
the  disease  is  seldom  if  ever  called  for ;  it  is  only  when 
there  are  symptoms  of  right  ventricle  failure,  and  then 
only  after  free  purgation  and,  if  necessary,  venesection 
have  been  employed,  that  it  should  be  prescribed.  Up 
to  a  certain  point  in  such  cases  its  influence  is  often  most 
beneficial,  but  sometimes  it  fails  to  relieve,  and  even 
appears  to  aggravate  the  symptoms.  If  continued  too 
long  in  cases  where  it  has  been  of  signal  service,  un- 
favourable effects  may  supervene,  marked  by  slowing  of 
the  pulse,  a  sense  of  precordial  oppression,  and  by  coupled 
heart-beats,  the  first  of  which  alone  reaches  the  wrist,  the 
second  being  unaccompanied  by  an  aortic  second  sound. 

In  many  cases  the  coupled  heart-beats  with  two  beats 
of  the  heart  to  one  beat  of  the  pulse  at  the  wrist  can  be 
induced  at  will  by  the  administration  of  digitalis. 

Digitalis,  therefore,  must  be  employed  with  caution  in 
mitral  stenosis,  and  its  effects  should  be  carefully  watched. 
Under  no  circumstances  should  it  be  prescribed  unless  the 
patient  is  under  observation,  and  it  should  rarely  be  given 
for  a  long  period  of  time. 

Nitro-glycerine  and  other  vasodilators  may  sometimes 
be  given  with  good  effect  for  many  weeks  or  even  months 
in  conjunction  with  general  tonics,  such  as  iron,  quinine, 
and  nux  vomica. 


CHAPTEK  XIII. 

VALVULAE   DISEASE   OF   THE   EIGHT    SIDE   OF 
THE  HEAET. 

TRICUSPID  INCOMPETENCE  AND  STENOSIS — PULMONIC  INCOM- 
PETENCE AND  STENOSIS — SYSTOLIC  PULMONIC  MURMURS 
WHICH  DO  NOT  INDICATE  STENOSIS. 

Primary  tricuspid  valvular  disease  is  rare,  aud  for  the 
most  part  is  congenital. 

Tricuspid  regurgitation  is  so  common  when  the  right 
ventricle  is  overdistended  by  violent  exertion  (the  so- 
called  safety-valve  action)  that  it  may  be  looked  on  as 
physiological ;  it  is  not  usually  attended  with  a  murmur. 
Tricuspid  incompetence,  again,  with  or  without  a  murmur, 
is  an  early  and  almost  constant  effect  of  back  pressure 
through  the  lungs  when  there  is  serious  valvular  disease 
of  the  left  ventricle.  In  both  instances  the  cause  of  the 
regurgitation  is  dilatation  of  the  right  ventricle,  temporary 
or  permanent,  as  the  case  may  be. 

The  tricusjnd  valve  may,  however,  be  damaged  during 
intra-uterine  life,  or  more  rarely  in  childhood  or  adolescence 
by  endocarditis  of  rheumatic  origin,  or,  where  serious 
valvular  disease  of  the  left  ventricle  exists,  may  undergo 
thickening  and  contraction  from  chronic  inflammation  set 
up  by  the  irritation  and  undue  strain  caused  by  protracted 
high  pressure  in  the  pulmonary  circulation. 

The  murmur  attending  tricuspid  regurgitation  is  systolic 


TRICUSPID  INCOMPETENCE.  201 

in  time  and  is  usually  blowing  in  character,  having  its 
maximum  intensity  about  one-third  of  the  distance  between 
the  left  edge  of  the  sternum  and  the  vertical  nipple  line. 
It  is  usually  audible  outwards  towards  the  apex,  and 
sometimes  at  the  apex  itself,  where  it  may  be  mistaken  for 
a  mitral  murmur.  Such  a  murmur,  when  constant  and 
not  occasional  only,  may  be  looked  on  as  indicative  of 
definite  tricuspid  insufficiency,  with  probably  actual  change 
in  the  valvular  flaps  and  chordae  tendineae.  A  musical 
tricuspid  systolic  murmur  may  sometimes  be  heard  over 
a  limited  area,  but  it  seldom  has  any  important  significance. 

It  is  not,  however,  from  the  character  of  the  murmur, 
or  from  its  presence,  that  conclusions  as  to  the  degree  of 
tricuspid  incompetence  are  to  be  drawn.  More  important 
information  is  gained  from  the  condition  of  the  veins  of 
the  neck  and  from  enlargement  of  the  liver.  The  veins 
of  the  neck  are  more  or  less  distended  according  to  the 
degree  of  regurgitation,  and  the  external  jugulars  may 
attain  even  the  size  of  the  little  finger.  Frequently  they 
will  fill  from  below  when  emptied  by  pressure. 

Pulsation  is  usually  present  when  there  is  much  regurgi- 
tation, and  is  often  very  conspicuous.  It  is  sometimes  seen 
to  be  double,  the  contraction,  first  of  the  auricle,  then  of 
the  ventricle,  sending  a  reflux  wave  along  the  jugulars. 
At  times  the  pulsation  in  the  internal  jugular  vein  is  so 
marked,  and  extends  so  high,  that  at  first  sight  it  may  be 
taken  for  the  carotid  throb  of  aortic  regurgitation ;  but  it 
is  of  course  easily  extinguished  by  light  pressure. 

The  effect  of  tricuspid  incompetence,  causing  damming 
back  of  the  blood  in  the  inferior  vena  cava,  is  felt  by 
the  liver,  which  gradually  becomes  much  congested  and 
enlarged,  and  eventually  may  pulsate  as  the  reflux  becomes 
considerable. 


HEART  DISEASE. 


Tricuspid  Stenosis. 


Tricuspid  stenosis  is  of  rare  occurrence,  and  is  usually 
associated  with  mitral  stenosis.  It  seldom,  if  ever,  occurs 
as  an  isolated  valvular  lesion.  It  is  in  most  cases  the  result 
of  an  attack  of  endocarditis  affecting  mitral  and  tricuspid 
valves  simultaneously,  and  is  rarely  a  congenital  affection. 

The  most  characteristic  physical  sign,  when  it  can  be 
recognized,  is  a  presystolic  murmur,  audible  in  the  tricuspid 
area,  but  it  is  not  always  present,  and  when  present  is 
not  easily  distinguished  from  a  concurrent  mitral  presystolic 
murmur.  In  many  cases  in  which  tricuspid  stenosis  has 
been  diagnosed  from  the  symptoms  during  life  and  found 
on  post-mortem  examination,  and  when  consequently  the 
presystolic  murmur  has  been  carefully  and  perseveringly 
sought  for  over  a  long  period,  it  has  been  impossible  to 
recognize  and  distinguish  it.  There  can  be  no  doubt, 
however,  that  the  murmur  has  been  frequently  heard  and 
recognized.  Another  important  physical  sign  of  tricuspid 
obstruction  is  distension  of  the  jugular  veins  with  little 
or  no  pulsation.  Mackenzie*  of  Burnley  has  obtained 
graphic  records  of  jugular  pulsation,  and  describes  an 
auricular  and  ventricular  type :  when  the  right  side  of 
the  heart  is  distended,  the  double  jugular  pulsation — the 
first  wave  auricular  and  the  second  ventricular — is  frequently 
very  distinct.  But  if  the  tricuspid  valves  are  contracted 
and  rigid  and  the  orifice  narrowed,  the  ventricular  wave  is 
cut  off,  while  the  auricular  may  be  present.  If,  however, 
the  auricle  is  paralyzed  by  over-distension,  the  auricular 
wave  may  also  be  missing. 

When  any  considerable  degree  of  tricuspid  stenosis 
exists,  the  symptoms  of  embarrassment  of  the  circulation 
and  of  venous  back  pressure  are  present  in  a  marked 
degree.      When    it    supervenes    on    mitral   stenosis   it    is 

*  Edin.  Hosp.  Reports,  189A,  vol.  ii. 


AFFECTIONS  OF  PULMONIC    VALVES.  203 

possible  that  it  has  a  beneficial  effect  in  postponing  the 
supervention  of  and  limiting  the  degree  of  tricuspid  re- 
gurgitation, but  this  is  doubtful.  The  symptoms  are 
usually  severe.  Cyanosis  and  dyspnoea  are  prominent 
features,  and  cedema  of  the  legs  is  commonly  present. 

The  Pulmonic  Valves. 

Disease  of  the  pulmonic  semilunar  valves  is  rare,  and 
of  the  two  conditions,  insufficiency  and  stenosis,  the  former 
is  the  more  uncommon. 

Pulmonic  insufficiency  gives  rise  to  a  diastolic  murmur, 
best  heard  in  the  left  third  intercostal  space,  and  conducted 
downwards.  It  must,  however,  be  borne  in  mind  that  the 
murmur  of  aortic  regurgitation  is  also  frequently  heard 
at  this  spot,  so  that  before  venturing  on  a  diagnosis 
of  pulmonic  regurgitation,  it  must  be  ascertained,  not 
only  that  the  pulmonic  second  sound  is  impaired,  but 
also  that  the  carotid  throb  and  collapsing  pulse  are 
absent,  and  that  the  aortic  second  sound  is  unimpaired. 
No  special  train  of  symptoms  can  be  attributed  to 
pulmonic  regurgitation. 

Pulmonic  stenosis  is  nearly  always  a  congenital  defect, 
and  as  it  is  fully  discussed  in  the  chapter  on  Congenital 
Malformations,  little  need  be  said  here.  The  murmur  to 
which  it  gives  rise  is  systolic  in  time  and  usually  loud  and 
rough,  varying  in  intensity.  It  is  most  distinct  in  the 
third  left  space,  about  three-quarters  of  an  inch  from 
the  margin  of  the  sternum,  but  it  is  conducted  along  the 
branches  of  the  pulmonary  artery  and  is  often  audible  over 
the  whole  cardiac  area  and  far  beyond,  sometimes  over  the 
entire  chest,  front  and  back.  Pulmonic  stenosis  is  often 
associated  with  some  other  congenital  defect,  such  as  a 
perforate  interventricular  septum  or  patent  foramen  ovale. 
When  the  last-named  condition  exists  cyanosis  is,  in  the 


204  HEART  DISEASE. 

majority  of  cases,  present  in  a  more  or  less  pronounced 
degree,  or  is  easily  induced  by  exertion. 

Systolic  pulmonic  murmurs  are  very  common  without 
change  in  the  orifice  or  valves. 

A  pulmonic  murmur  may  be  present  in  a  patient 
suffering  from  anaemia  and  disappear  as  the  blood  regains 
its  normal  character ;  it  is  then  properly  termed  "  hseniic." 

Again,  a  murmur  in  this  situation  may  be  induced  by 
severe  or  protracted  exertion,  and  last  for  some  hours  or 
days.  There  will  probably  be  at  the  same  time  indica- 
tions of  dilatation  of  the  right  ventricle,  though  it  is  not 
easy  to  explain  how  this  could  give  rise  to  the  pulmonic 
murmur. 

A  third  variety  of  systolic  murmur  in  the  pulmonic 
area,  which  may  be  loud  and  rough,  and  often  varies 
greatly  in  the  same  subject  and  without  obvious  cause, 
or  especially  on  change  of  position,  is  not  unfrequently 
met  with  in  adolescents  of  both  sexes,  which  cannot  be 
attributed  to  anaemia  or  to  dilatation  of  the  right  ventricle. 
It  is  not  indicative  of  temporary  weakness  or  organic 
unsoundness  of  heart,  nor  is  it  incompatible  with  capacity 
fur  vigorous  and  sustained  exertion,  as  boys  and  men  in 
whom  it  is  present  can  play  football  and  train  for  races 
with  impunity.  Its  presence  may  be  made  a  pretext  for 
rejecting  candidates  for  the  army  on  medical  grounds,  but 
I  have  known  many  men  in  whom  such  a  murmur  was 
present  go  through  arduous  campaigns  without  breaking 
down.  I  have  never  known  such  a  murmur  develop  into 
actual  heart  disease ;  on  the  contrary,  it  usually  disappears 
in  adult  life,  except  now  and  then  in  women. 

The  causation  of  such  a  murmur  is  apparently  as 
follows.  Usually  the  conus  arteriosus  of  the  pulmonary 
artery  is  covered  by  the  thin  edge  of  the  overlapping  left 
lung.  In  the  cases  under  consideration  the  covering  by 
lung  is   incomplete,  and  a  part  of  the   conus  comes  into 


PULMONIC  MURMURS.  205 

contact  with  the  chest  wall,  and  during  systole  is  flattened 
more  or  less  against  the  chest  wall.  An  eddy  is  thus 
formed  in  the  current  of  blood  rushing  into  the  pulmonary 
artery,  which  gives  rise  to  a  murmur.  Evidence  in  support 
of  this  explanation  is  afforded  by  the  fact  that  the  murmur 
usually  disappears  when  the  patient  is  told  to  take  a  deep 
breath  and  hold  it,  as  a  cushion  of  lung  is  then  brought 
over  the  conus  arteriosus  between  it  and  the  chest  wall. 
The  result  is  the  more  striking  if  the  murmur  haprjens  to 
be  loud  and  vibratory. 


CHAPTEE   XIY. 
CONGENITAL   MALFORMATIONS. 

VARIETIES  OP  CONGENITAL  MALFORMATIONS — RELATIVE 
FREQUENCY  OF  OCCURRENCE  —  OF  SINGLE  AND  COMBINED 
DEFECTS —  PHYSICAL  SIGNS  —  SYMPTOMS  —  CYANOSIS — 
CAUSE  OF  CYANOSIS — DIAGNOSIS — PROGNOSIS. 

Some  of  the  most  important  varieties  of  congenital  mal- 
formations of  the  heart  and  great  vessels  are — 

1.  The  heart  consisting  of  two  or  three  cavities,  the 
interventricular  or  interauricular  septum,  or  both,  being 
absent.     This  is  of  rare  occurrence. 

2.  Incomplete  interventricular  septum,  usually  taking 
the  form  of  a  perforation  in  the  upper  third  of  the 
septum. 

3.  Patent  foramen  ovale. 

4.  Persistence  of  patent  ductus  arteriosus. 

5.  Stenosis  of  the  pulmonary  orifice  due  to  constriction 
of  the  trunk  of  the  vessel  itself,  or  of  the  infundibular 
portion  of  the  right  ventricle,  or  to  the  adhesion  or 
malformation  of  the  valves. 

6.  Transposition  of  pulmonary  artery  and  aorta. 

7.  The  aorta  and  pulmonary  artery  may  both  arise  from 
the  same  ventricle. 

8.  Malformations  of  the  aortic,  tricuspid,  or  mitral 
valves  are  not  of  common  occurrence.  In  most  cases,  where 
the  tricuspid  valve  is  found  to  be  affected  at  birth,  the 
probabilities  will  be  that  it  has  been  damaged  by  endo- 
carditis occurring  during  foetal  life. 


CONGENITAL   MALFORMATIONS.  207 

Pulmonic  Stenosis. — Of  these  varieties  by  far  the  most 
common  is  stenosis  of  the  pulmonary  orifice.  Of  181  cases 
of  congenital  malformation  collected  by  Peacock,  in  90 
more  or  less  contraction  of  the  pulmonary  orifice  was 
present,  and  in  29  others  the  orifice  or  trunk  of  the  vessel 
was  obliterated.* 

The  narrowing  may  be  due  to  constriction  of  the  conus 
arteriosus  above  the  valves,  or  to  adhesion  between  the 
cusps  of  the  valves.  The  artery  may  be  very  small  and 
ill  developed  and  the  valves  present  but  impervious. 

The  most  common  varieties  of  congenital  heart  disease, 
after  pulmonic  stenosis,  are  deficiency  of  the  interventricular 
septum  and  patency  of  the  foramen  ovale. 

Deficiency  of  the  interventricular  septum  usually  takes 
the  form  of  a  perforation  in  the  upper  third  of  the 
septum,  in  the  undefended  or  membranous  space,  so  called 
because  normally  the  septum  here  only  consists  of  two 
layers  of  endocardium.  It  is  rare  as  an  isolated  lesion,  but 
is  not  uncommon  in  association  with  other  malformations 
which  give  rise  to  unequal  pressure  in  the  two  ventricles. 
For  instance,  it  is  frequently  found  coexisting  with  pul- 
monic stenosis,  in  which  the  pressure  in  the  right  ventricle 
is  in  excess  of  that  in  the  left.  Not  unfrequently  in  such 
cases  the  right  ventricle  is  greatly  hypertrophied  and  the 
septum  is  deviated  to  the  left,  and  in  some  cases  the  aorta 
arises  wholly  or  in  part  from  the  right  ventricle. 

Patency  of  the  foramen  ovale  may  occur  in  connection 
with  pulmonic  stenosis ;  but  this  cannot  be  always  attributed 
to  excess  of  pressure  in  the  right  auricle,  as  it  is  sometimes 
found  as  an  isolated  lesion;  and  also  cases  are  recorded 
in  which  the  foramen  was  found  closed,  though  excess  of 
pressure  must  have  existed  in  the  right  auricle. 

The  ductus  arteriosus  may  remain  patent  in  consequence 
of  some  obstruction  to  the  passage  of  blood  through  the 

*  Peacock,  "Malformations  of  the  Human  Heart,"  p.  193. 


208  HEART  DISEASE. 

lungs  or  systemic  vessels ;  not  infrequently  a  patent  ductus 
arteriosus  occurs  in  association  with  a  patent  foramen 
ovale,  the  patency  of  both  being  due  to  similar  causes  : 
hence  the  two  may  be  found  together  with,  and  as  a  direct 
result  of,  pulmonic  stenosis. 

In  a  case  recently  under  my  care  at  St.  Mary's  Hospital, 
patency  of  the  ductus  arteriosus  existed  as  an  isolated 
lesion. 

Transposition  of  Pulmonary  Artery  and  Aorta. — The  aorta 
may  arise  from  the  right  ventricle,  and  the  pulmonary 
artery  from  the  left.  The  ductus  arteriosus  will  usually 
remain  patent.  The  aorta  and  pulmonary  artery  may  both 
arise  from  the  same  ventricle.  In  a  specimen  in  the  St. 
Mary's  Hospital  Museum,  both  aorta  and  pulmonary  artery 
arise  from  the  right  ventricle.  The  interventricular  septum 
is  absent  in  the  upper  third,  so  that  there  is  free  com- 
munication between  the  two  ventricles.  The  right  ventricle 
is  greatly  dilated  and  hypertrophied  and  the  left  very 
small.  The  pulmonary  artery  is  very  small  and  ill 
developed,  and  its  lumen  is  only  about  2  mm.  in  diameter. 

In  spite  of  this  the  child  from  which  the  specimen  was 
taken  lived  to  the  age  of  three  months,  though  cyanosed 
and  dyspnoeic  from  birth,  and  very  poorly  developed. 

Physical  Signs. 

In  pulmonic  stenosis  a  loud,  rough,  systolic  murmur  is 
usually  to  be  heard  over  the  precordial  region  with  its 
maximum  intensity  at  the  level  of  the  nipple,  midway 
between  the  nipple  and  the  sternum.  It  will  be  conducted 
along  the  branches  of  the  pulmonary  artery  so  that  it 
will  be  heard  over  a  large  area  on  both  sides  of  the  chest ; 
but  it  will  be  heard  more  distinctly  on  the  left  side  of  the 
chest  between  the  base  of  the  heart  and  the  clavicle  than 
over  the  aorta.  In  association  with  this  the  right  ventricle 
will  usually  be  hypertrophied. 


CONGENITAL  MALFORMATIONS.  209 

Deficiency  of  the  interventricular  septum  may  give  rise 
to  a  systolic  murmur  whose  seat  of  maximum  intensity 
is,  according  to  Roger  and  Potain,  in  the  fourth  left  space 
half  an  inch  above  the  nipple ;  but  as  this  defect  commonly 
coexists  with  pulmonic  stenosis,  such  a  murmur  would 
probably  be  masked  by  that  due  to  the  pulmonic  lesion. 
A  murmur  that  may  occur  in  cases  of  deficient  inter- 
ventricular septum,  and  which  I  look  upon  as  diagnostic, 
is  one  quite  different  in  character  to  any  that  occur  in 
the  usual  forms  of  valvular  disease.  It  is  harsh  and  loud, 
but  its  great  peculiarity  is  that  it  never  ceases,  becoming 
suddenly  louder  and  higher  pitched  with  the  systole, 
and  subsiding  into  a  continuous  rumble  during  diastole, 
reminding  one  of  the  kind  of  noise  of  varying  intensity 
made  by  a  knife-grinder's  wheel  when  a  knife  is  being 
sharpened. 

Patent  foramen  ovale. — There  is  no  known  auscultatory 
or  other  physical  sign  by  which  a  patent  foramen  ovale 
can  be  diagnosed.  Peacock  quotes  one  case  of  patent 
foramen  ovale  without  other  defect,  in  which  the  patient, 
a  girl,  lived  to  the  age  of  sixteen,  when  she  died  of 
pulmonary  tuberculosis.  There  was  no  cyanosis,  and  till 
she  began  to  suffer  from  tuberculosis  there  were  no 
symptoms  other  than  those  of  general  debility.  In  a 
case  under  my  care  the  patient  was  a  man,  who  died  at 
the  age  of  thirty  from  bronchitis.  There  was  no  marked 
cyanosis  during  infancy,  there  were  no  special  symptoms 
of  morbus  cordis,  and  no  cardiac  murmurs ;  the  patient 
was,  however,  dull  and  of  sluggish  intellect,  but  could 
take  long  walks  without  seeming  distressed  in  any  way, 
or  appearing  the  worse  for  it.  During  the  fatal  attack 
of  bronchitis  cyanosis  developed,  attended  with  torpor.  A 
noteworthy  point  was  that  the  cyanosis  deepened  during 
sleep,  and  there  was  no  spontaneous  waking  up,  and  the 
patient  was  roused  with  difficulty.     Eventually  the  torpor 


2io  HEART  DISEASE. 

and  cyanosis  deepened  into  fatal  coma.     At   the   autopsy 
the  only  cardiac  lesion  found  was  a  patent  foramen  ovale. 

Patent  Ductus  Arteriosus.  —  This  usually  is  found  asso- 
ciated with  other  lesions  of  which  it  may  be  difficult  to 
differentiate  the  physical  signs.  I  have  recently,  however, 
had  under  my  care  a  case,  already  referred  to,  in  which 
patency  of  the  ductus  arteriosus  existed  as  an  isolated 
lesion  The  only  physical  sign  was  a  soft  blowing  systolic 
murmur  of  moderate  intensity  audible  over  most  of  the 
cardiac  area,  most  marked  in  the  third  left  intercostal 
space ;  it  diminished  in  intensity  towards  the  clavicle  and 
towards  the  aortic  area,  but  was  very  distinct  at  the  apex. 
There  was  no  cyanosis,  and  there  were  no  symptoms 
directly  attributable  to  the  condition,  but  the  child  died  of 
diarrhoaa  and  vomiting.     It  was  7  months  old. 

Symptoms. 

The  child  suffering  from  a  serious  congenital  affection 
of  the  heart  is  usually  irritable  and  fretful,  and  may  be 
subject  to  fits.  The  fingers  and  toes  are  clubbed,  and  the 
extremities  cold.  He  may  be  always  cyanosed  to  a  varying 
degree,  or  only  become  cyanosed  on  exertion.  There  will 
usually  be  constant  shortness  of  breath,  and  paroxysms  of 
dyspnoea  may  occur,  in  which  cyanosis  becomes  so  intense 
that  the  extremities  become  almost  black.  He  will  remain 
stunted  in  growth  and  backward  in  development,  intel- 
lectually as  well  as  physically.  The  symptoms  will  of 
course  vary,  according  to  the  nature  of  the  lesion.  They 
will  be  most  marked  in  a  case  of  severe  pulmonary  stenosis, 
and  may,  as  has  already  been  seen,  be  entirely  absent  in  a 
case  of  uncomplicated  patent  foramen  ovale. 

Cyanosis. — In  many  instances  of  congenital  malforma- 
tion of  the  heart,  the  most  marked  and  striking  feature  is 
the  cyanosis   of  the  patient ;   hence  the   various  forms  of 


CONGENITAL  MALFORMATIONS.  21  i 

congenital  heart  disease  have  been  grouped  together  under 
the  names  morbus  cceruleus,  or  blue  disease,  by  English, 
and  cyanose,  or  maladie  bleue,  by  French  authors. 

The  explanation  of  the  cause  of  this  peculiar  discolora- 
tion is  still  a  matter  of  dispute.  Senac,  Corvisart,  Gintrac, 
and  others  attribute  it  to  the  mixture  of  arterial  and 
venous  blood  in  the  heart  or  great  vessels,  owing  to  defec- 
tive septa  or  patent  ductus  arteriosus.  Cruveilhier  at- 
tributed it  to  venous  congestion.  It  has  been  proved, 
however,  that  cyanosis  may  exist  without  the  intermixture 
of  currents  of  blood,  also  that  complete  intermixture  may 
take  place  without  the  occurrence  of  cyanosis. 

It  is  obvious,  therefore,  that  neither  of  these  explana- 
tions are  sufficient.  Stille,  with  a  view  to  determining  the 
cause  of  cyanosis,  collected  77  cases  of  congenital  morbus 
cordis  in  which  cyanosis  was  present.  In  53  instances 
the  pulmonary  artery  was  constricted  or  impervious,  or 
its  orifice  was  obstructed  in  some  way.  He  came  to  the 
conclusion,  therefore,  that  cyanosis  was  due  to  venous 
congestion  usually  dependent  on  obstruction  at  the  orifice 
of  the  pulmonary  artery,  or  on  some  other  cause  giving 
rise  to  obstruction  to  the  venous  return.  This  is  clearly 
not  a  complete  explanation,  as  there  is  often  no  cyanosis 
in  cases  of  morbus  cordis  in  adults  where  the  venous 
congestion  is  extreme.  Peacock  makes  another  important 
suggestion,  that  deficient  aeration  of  the  blood  is  a  con- 
tributory cause  of  cyanosis ;  he  says,  "  where  only  a  small 
proportion  of  the  blood  is  submitted  at  one  time  to 
aeration  in  the  lungs,  the  whole  mass  must  be  of  a  dark 
colour,  consequently  the  hue  of  the  surface  will  be  pro- 
portionately dark."  This  is  especially  the  case  in  pulmonic 
stenosis,  and  Stille's  statistics,  which  show  that  pulmonic 
stenosis  is  the  commonest  cause  of  cyanosis,  afford  strong 
support  to  this  view,  that  aeration  of  a  small  proportion 
only  of  the  blood  is  the  essential  cause  of  cyanosis. 


HEART  DISEASE 


Diagnosis. 


Though  in  severe  cases  it  is  usually  easy  to  arrive 
at  a  diagnosis  of  congenital  heart  disease  from  a  history 
of  cyanosis  and  dyspnoea  since  birth,  with  the  clubbing 
of  the  fingers  and  toes,  it  is  difficult  and  in  many  instances 
impossible  to  be  certain  of  the  exact  nature  of  the 
malformation. 

Where  with  a  history  of  cyanosis  and  paroxysms  of 
dyspnoea  since  birth  we  find  a  loud,  rough,  systolic  murmur, 
with  its  maximum  intensity  on  the  left  side  at  the  level 
of  the  nipple,  midway  between  the  nipple  and  sternum, 
together  with  a  hypertrophied  right  ventricle,  we  may 
be  fairly  certain  that  pulmonary  stenosis  is  the  main 
lesion;  but  whether  a  patent  foramen  ovale  or  perforate 
interventricular  septum,  or  patent  ductus  arteriosus,  is 
present  as  well,  it  will  often  be  impossible  to  decide. 

Prognosis. 

The  lesion  is  in  this  case  stationary,  and  not  pro- 
gressive, but  the  malformations  being  widely  different, 
the  effect  they  have  on  the  duration  of  life  will  vary 
considerably. 

1.  In  cases  of  moderate  constriction  of  the  pulmonary 
artery  without  other  malformation,  for  which  hypertrophy 
of  the  right  ventricle  is  sufficient  to  compensate,  there 
will  be  no  cyanosis,  and  the  patient  may  live  many  years 
without  serious  inconvenience,  except  on  violent  exertion. 

2.  In  cases  where  the  foramen  ovale  is  open  the 
pulmonary  stenosis  is  usually  greater,  and  hence  the 
duration  of  life  will  probably  be  less ;  but  out  of  20  cases 
which  Peacock  collected,  11  lived  to  the  age  of  15  years 
and  over,  1  living  to  the  age  of  57. 

3.  Where  with  pulmonary  stenosis  the  interventricular 


CONGENITAL   MALFORMATIONS.  213 

septum  is  also  deficient,  the  prognosis  is  much  less 
favourable,  for  not  only  must  the  pulmonary  constriction 
be  considerable  to  have  given  rise  to  this  deficiency,  but, 
further,  in  such  case  the  aorta  usually  arises  in  part  from 
the  right  ventricle.  Of  64  such  cases  collected  by  Peacock, 
only  14  survived  the  age  of  15.  If,  however,  the  degree 
of  pulmonic  stenosis  is  slight  and  the  perforation  in  the 
septum  small,  life  may  be  prolonged,  and  two  patients  are 
now  living,  at  the  age  of  30  or  upwards,  in  which  I  believe 
this  condition  to  exist ;  one  has  borne  a  child. 

4.  Where  the  pulmonary  artery  is  impervious,  the 
duration  of  life  rarely  exceeds  a  few  months,  though  of  28 
such  cases  of  Peacock's,  3  lived  to  the  age  of  9  or  10,  and 
1  to  12  years. 

In  a  case  under  the  care  of  Dr.  Cheadle  in  St.  Mary's 
Hospital  in  1902,  a  child  lived  to  the  age  of  14  months  with 
an  impervious  pulmonary  artery  and  a  heart  consisting  of 
only  two  cavities,  an  auricle  and  ventricle.  It  was  cyanosed 
and  dyspnoaic  from  birth. 

5.  Transposition  of  the  main  arteries,  or  arrest  of 
development,  so  that  the  heart  consists  of  two  or  three 
cavities  only,  is  usually  incompatible  with  life  for  any 
long  period  after  birth,  but  4  cases  are  recorded  by  Peacock 
where  with  one  ventricle  only  and  two  auricles  persons 
lived  to  the  ages  of  11,  16,  23,  and  24  years  respectively. 

6.  Patency  of  the  foramen  ovale  uncomplicated  by  any 
other  defect  may  not  of  itself  give  rise  to  any  serious 
symptoms;  doubtless  in  most  instances  where  the  opening 
is  valve-like  it  will  become  closed  before  adolescence  is 
reached.  Where  it  persists  or  allows  of  extensive  leakage, 
any  lung  affection,  such  as  bronchitis,  which  tends  to 
increase  the  pressure  in  the  right  side  of  the  heart  and 
cause  a  flow  of  non-aerated  blood  from  the  right  to  the 
left  auricle,  will  be  especially  dangerous  and  liable  to 
prove  fatal. 


CHAPTER  XY. 

PROGNOSIS   IN   VALVULAR    DISEASE 
(GENERAL). 

the  nature  op  the  lesion  :  the  relative  danger 
attaching  to  each  particular  lesion — sudden 
death:  the  valvular  diseases  in  which  it  is 
liable  to  occur — the  extent  of  the  lesion  — 
the  stationary  or  progressive  character  of  the 
lesion  as  influencing  prognosis. 

In  cases  of  heart  disease,  prognosis  is  of  special  im- 
portance, since  a  patient  who  knows  that  he  is  suffering 
from  some  affection  of  the  heart  immediately  dreads  the 
worst.  It  is  always  necessary  to  allay  his  fears  as  far 
as  possible,  as  these  in  themselves  tend  to  aggravate  the 
danger  attending  the  disease.  In  some  cases  this  may 
be  done  with  absolute  confidence ;  in  others,  the  appre- 
hensions may  be  only  too  well  founded  ;  in  others,  again, 
the  issue  may  be  uncertain  and  may  be  dependent  on  other 
conditions  than  the  state  of  the  heart.  It  will  be  most 
important  in  all  instances  that  the  medical  attendant  should 
form  a  definite  idea  of  the  probable  effect  the  heart  disease 
will  have  in  shortening  life,  so  that  he  may  guide  the 
patient  and  his  friends  in  making  arrangements  on  which 
the  welfare  of  the  family  may  depend. 

The  following  are  the  points  which  should  specially  be 
considered  in  regard  to  prognosis  :  — 

1.  The  valve  affected  and  the  relative  danger  attaching 
to  the  particular  lesion. 


RELATIVE  DANGER   OF   VALVULAR  LESIONS.  215 

2.  The  extent  of  the  lesion. 

3.  The  stationary  or  progressive  character  of  the  lesion. 

4.  The  degree  of  soundness  and  vigour,  functional  and 

nutritional,  of  the  muscular  substance  of  the  heart, 
of  the  arterial  walls,  and  of  the  tissues  generally. 

5.  The  age  of  the  patient. 

6.  The  family  history,  especially  in  regard  to  whether 

there  is  any  hereditary  tendency  to  heart  disease. 

7.  The  habits  and  mode  of  life  of  the  patient. 

8.  The  presence  or  absence  of  other  diseases — such  as 

anaemia,    bronchitis,    renal    affections — as    compli- 
cations. 

The  Relative  Danger  attaching  to  the  Different 
Valvular  Lesions. 

According  to  Walshe,  the  valvular  affections  stand  in 
the  order  of  relative  gravity  as  follows  :  tricuspid  regurgi- 
tation, mitral  regurgitation,  mitral  constriction,  aortic 
regurgitation,  pulmonary  constriction,  aortic  constriction. 
Tricuspid  regurgitation,  however,  as  has  already  been  said, 
is  rarely  primary,  but  usually  occurs  as  a  result  of  obstruction 
to  the  transit  of  blood  through  the  lungs  either  from  disease 
in  these  organs,  or  from  valvular  disease  in  the  left  side  of 
the  heart.  It  is  therefore  an  effect  of  serious  valvular 
lesions  of  the  left  side  of  the  heart,  and  can  scarcely  be 
regarded  as  a  cause  of  the  fatal  termination. 

My  own  experience  would  lead  me  to  modify  Walshe's 
arrangement  somewhat,  and  to  give  this  order  of  relative 
danger  :  aortic  incompetence,  mitral  stenosis,  aortic  stenosis, 
mitral  incompetence.  Aortic  incompetence  is  most  rapidly 
fatal  when  it  comes  on  late  in  life  at  a  period  when  com- 
pensatory hypertrophy  is  established  with  difficulty,  more 
especially  when  due  to  degenerative  change  in  the  valves. 
In  childhood  and  early  adolescence,  mitral  stenosis  is  often 
more    serious    than    aortic    incompetence,    owing    to    the 


216  HEART  DISEASE. 

progressive  nature  of  the  lesion  and  to  imperfect  develop- 
ment of  the  left  ventricle.  It  is,  however,  difficult  to 
estimate  with  any  accuracy  the  relative  danger  of  different 
valvular  lesions,  as  so  many  other  factors  must  he  taken 
into  consideration  in  prognosis. 

Sudden  Death. 

One  of  the  first  questions  to  be  discussed  is  the  liability 
to  sudden  death  in  heart  disease.  In  the  mind  of  the 
general  public,  disease  of  the  heart  and  sudden  death  are  so 
closely  associated  that  the  mention  of  the  one  immediately 
suggests  the  other,  and  in  a  nervous  patient,  a  pain  or  a 
sense  of  weight  or  oppression  in  the  cardiac  region,  easily 
exaggerated  by  the  concentration  of  his  attention  upon  the 
heart,  will  make  him  think  the  end  is  near. 

It  is  therefore  of  the  greatest  importance  that  we  should 
know  with  certainty,  in  what  form  of  heart  disease  sudden 
death  is  liable  to  occur,  and  be  able  in  cases  where  no  such 
danger  exists  to  say  so  with  confidence.  It  must  be  under- 
stood that  the  sudden  death  under  consideration  is  such  as  is 
meant  by  the  familiar  phrase  "  dropping  down  dead,"  with 
little  or  no  warning,  the  individual  having  been  up  to  the 
moment  in  apparent  health,  or  so  far  well  as  to  be  able  to  go 
about  his  duties,  or  at  any  rate  not  suffering  from  dropsy  or 
other  serious  symptoms  of  cardiac  embarrassment. 

In  all  forms  of  heart  disease,  when  the  effects  on  the 
circulation  have  become  very  decided,  and  such  symptoms 
as  engorgement  of  the  lungs,  with  dyspnoea,  dropsy,  effusion 
into  the  pleural  cavities,  albuminuria,  have  set  in,  the  final 
struggle  may  come  on  abruptly  and  end  speedily.  This, 
however,  is  not  the  mode  of  death  which  is  the  special 
dread  attending  heart  disease. 

Walshe,  in  speaking  of  the  different  forms  of  valvular 
lesions,  says  that  only  one  causes  sudden  death,  namely, 
aortic  incompetence. 


SUDDEN  DEATH.  217 

In  a  paper  read  before  the  Harveian  Society  in  1866, 
I  gave  as  the  conclusion  at  which  I  had  arrived  that 
"  sudden  death  is  a  contingency  which  may  almost  be  left 
out  of  consideration  in  valvular  disease,  except  in  aortic 
regurgitation."  This  would  still  express  very  nearly  my 
individual  experience.  As  will  be  shown  in  the  part  of  this 
book  on  the  structural  changes  in  the  wall  of  the  heart, 
there  are  other  conditions  more  likely  to  give  rise  to 
sudden  death  than  aortic  regurgitation.  Here,  however,  we 
are  considering  only  the  valvular  lesions. 

As  individual  experience  is  not  altogether  a  trustworthy 
guide,  some  years  ago  Sidney  Phillips,  at  my  request, 
went  through  the  post-mortem  records  of  St.  Mary's 
Hospital  of  four  hundred  cases  in  which  the  heart  had 
undergone  marked  change,  in  order  to  see  what  light  they 
threw  on  the  question  of  heart  disease  and  sudden  death. 
Of  these,  151  were  cases  of  valvular  disease,  204  examples  of 
changes  in  the  wall  of  the  heart.  Of  aortic  regurgitation 
there  were  thirty-eight  cases.  Three  were  brought  to  the 
hospital  dead,  a  fourth  died  in  the  hospital  suddenly  during 
convalescence  from  acute  rheumatism.  In  six  more  the 
final  symptoms  came  on  abruptly  and  were  rapidly  fatal, 
one  dying  within  twenty-four  hours  of  his  admission  to  the 
hospital,  another  within  two  days.  There  were  eleven 
examples  of  aortic  stenosis  without  one  sudden  death  in  the 
sense  of  the  patient  being  overtaken  by  death  while  in 
apparent  health  or  free  from  symptoms  arising  from  heart 
disease. 

Of  mitral  stenosis  there  were  fifty-three  instances.  One 
patient  only  was  brought  in  dead,  a  young  girl  who  was 
picked  up  in  the  street.  From  the  condition  of  the  lungs 
there  was  no  doubt  that  she  must  have  been  suffering 
severely  from  symptoms  due  to  the  heart  affection. 

Of  mitral  insufficiency  there  were  forty-nine  cases. 
Of  these,  two   may   be   said   to  have   died   suddenly,  but 


218  HEART  DISEASE. 

both  had  serious  symptoms  and  were  under  treatment  in 
hospital,  and  in  both  the  pericardium  also  was  universally 
adherent. 

In  three  more  a  final  attack  of  dyspnoea  set  in  abruptly 
and  proved  rapidly  fatal. 

These  numbers  are  not  given  as  representing  with 
anything  like  accuracy  the  proportion  of  sudden  deaths  in 
the  different  forms  of  valvular  disease,  but  they  afford 
confirmation  of  the  opinion  formed  from  personal  experience 
that  aortic  insufficiency  is  the  only  form  of  valvular  disease 
attended  with  danger  of  sudden  death. 


The  Extent  of  the  Lesion. 

In  a  previous  chapter  the  indications  by  means  of  which 
the  extent  of  the  lesion  may  be  estimated,  have  been 
discussed.  A  certain  limited  amount  of  information  on 
this  head  is  obtained  from  the  character  of  the  murmur. 
Further  help  is  derived  from  the  pulse,  and  still  more 
from  the  amount  of  hypertrophy  and  dilatation  which  the 
heart  has  undergone  in  consequence  of  the  lesion.  A 
valvular  murmur,  accompanied  by  dilatation  or  hypertrophy 
or  both,  is  attended  with  greater  danger  than  a  similar 
murmur  not  so  accompanied ;  not,  however,  because  the 
hypertrophy  and  dilatation  add  new  elements  of  danger,  but 
because  the  valvular  change  causing  the  murmur  has  given 
rise  also  to  mechanical  difficulty  when  these  changes  are 
present,  whereas  their  absence  shows  that  it  has  given  rise 
to  no  serious  obstacle  to  the  circulation. 

It  must  be  understood,  however,  that  when  hypertrophy 
and  dilatation  are  taken  as  a  measure  of  the  valvular  lesion 
it  is  in  the  absence  of  any  evidence  of  functional  inefficiency. 
Where,  in  addition  to  the  disease  of  the  valves,  there  is 
degeneration  of  the  muscular  substance  of  the  heart,  this 
will   give   rise   to  further   dilatation.      Still,  however,  the 


PROGNOSIS  ACCORDING    TO  ETIOLOGY  219 

amount  of  dilatation  may  be  taken  as  expressing  the 
relation  between  the  mechanical  difficulty  and  the  power  of 
the  heart  to  cope  with  it.  Naturally  the  more  extensive 
the  lesion,  as  estimated  by  the  changes  in  the  heart,  the 
more  serious  the  prognosis,  because  the  compensatory 
balance  has  been  established  with  difficulty  and  is  more 
easily  upset. 

The   Stationary   or   Progressive   Character  of  the 
Lesion  as  influencing  Prognosis. 

A  given  state  of  valve  existing— a  certain  degree  of 
obstruction  or  incompetence— it  will  be  obvious  that  the 
future  of  the  patient  will  be  very  greatly  influenced  by  the 
question  whether  the  morbid  process  which  has  damaged 
the  valve  is  still  in  progress,  or  has  come  to  a  standstill. 
In  the  one  case,  where  the  change  has  reached  its 
maximum,  we  know  what  we  have  to  deal  with — the 
hypertrophy  and  dilatation  give  an  approximate  idea  of  the 
functional  imperfection ;  they  compensate  it  or  they  do  not, 
and  the  prognosis  varies  accordingly :  in  the  other  there 
can  be  but  one  course  and  issue,  a  gradual  or  swift  aggra- 
vation of  symptoms,  unless  indeed  sudden  death  interferes. 

Such  a  difference  exists  arising  out  of  the  character  of 
the  pathological  process  by  which  the  valve  is  affected. 
Speaking  generally,  the  question  is  whether  the  valvular 
change  has  had  its  origin  in  an  acute  inflammatory 
attack  or  is  the  result  of  a  chronic  degenerative  process. 
Fortunately  the  distinction  is  for  the  most  part  easy. 

In  the  chapter  on  the  aetiology  of  valvular  disease  the 
various  causes  of  lesions  of  the  valves  and  orifices  have 
been  enumerated  and  briefly  discussed.  They  are,  acute 
endocarditis,  chronic  endocarditis,  and  degenerative  changes 
in  the  valves,  rupture  of  valve,  dilatation  of  the  orifice. 

Acute  Endocarditis. — When  the  valvular   lesion  can  be 


HEART  DISEASE. 


traced  definitely  to  an  attack  of  acute  endocarditis,  there 
is  this  favourable  element  in  the  prognosis,  that  the  lesion 
once  established  is  not  progressive.  If  the  lesion  was  slight 
it  remains  slight,  and  does  not  increase  in  severity  after 
the  endocarditis  has  subsided;  consequently  the  dilata- 
tion and  hypertrophy  of  the  heart  will  be  small,  if  indeed 
they  are  appreciable ;  if  the  lesion  is  extensive,  the  dilata- 
tion and  hypertrophy  which  will  follow  are  proportionate. 
Hence  we  are  able  to  arrive  at  a  definite  conclusion  as  to 
the  extent  of  the  lesion,  and  give  an  approximate  idea  as 
to  the  probable  effect  it  will  have  in  shortening  life,  and 
say  how  far  exercise  and  exertion  can  be  allowed.  The  only 
exception  to  be  made  will  be  in  cases  of  mitral  stenosis, 
where  the  orifice  may  become  gradually  further  narrowed 
after  the  initial  damage  has  been  done,  owing  to  cicatricial 
contraction  of  the  inflammatory  products. 

Chronic  Endocarditis. — The  fatal  feature  about  this 
chronic  inflammatory  or  degenerative  change  in  the  valves 
is,  that  once  begun  it  is  inevitably  progressive.  The  heart 
and  system  may  have  accommodated  themselves  to  a  degree 
of  obstruction  or  regurgitation,  but  this  does  not  remain 
the  same;  slowly  or  rapidly  the  valvular  lesion  will  in- 
crease, and  with  it  the  obstacle  to  the  due  transmission  of 
the  blood  through  the  heart.  This  takes  place  at  an  age 
when  the  heart  is  little  able  to  adapt  itself  to  change  or  to 
meet  the  increasing  difficulty,  and  is,  moreover,  itself  liable 
to  structural  decay ;  further,  the  cause  which  has  worn  out 
the  valves,  the  excessive  resistance  in  the  peripheral  circu- 
lation giving  rise  to  unduly  high  tension  in  the  arterial 
system,  is  probably  still  in  operation. 

Before,  however,  we  take  so  serious  a  view  of  any  given 
case  in  which  a  valvular  murmur  has  been  developed  late 
in  life,  and  accept  it  as  necessarily  indicative  of  progressive 
disease,  we  ought  to  make  sure  that  it  is  due  to  degenera- 
tive changes,  and  not  to  mere  roughening  of  the  valve.     To 


PROGNOSIS  IN  RUPTURE   OF  A    VALVE.  221 

prove  the  former  we  ought  to  have  evidence  of  actual 
damage  to  the  valve,  either  in  the  shape  of  symptoms 
traceable  to  functional  inefficiency  or  of  modifications  of 
the  physical  signs.  It  is  common  in  elderly  people  to  find 
a  mitral  or  aortic  systolic  murmur  develop,  which  persists 
for  years  without  any  symptoms  of  heart  disease,  due  to  a 
slight  roughness  or  rigidity  in  the  case  of  the  aortic  valve 
which  sets  up  vibrations  ;  or,  in  the  case  of  the  mitral  valve, 
to  a  little  thickening  or  want  of  pliability  which  prevents 
an  accurate  apposition  of  the  flaps  of  the  valve,  but  does 
not  allow  of  any  appreciable  regurgitation. 

Rupture    of    Valve. — Eupture    of    a   valve    is    of   rare 
occurrence    and   is    always    a   serious   lesion.      The    valve 
affected  is  usually  the  aortic,  and  the  sudden  and  severe 
strain  on  the  heart,  which  has  no  time   to  accommodate 
itself  to  the  altered  conditions  of  the  circulation,  leads  to 
dilatation  of  the  left  ventricle  and  the  consequent  onset 
of  severe  symptoms   when  the  rupture   of  a  cusp  is  com- 
plete.     The   accident   is  usually  accompanied  by  sudden 
pain  in   the    chest,    and  the  patient  may  be  seized  by  a 
syncopal   attack,  which   will    at    once    prove   fatal.      The 
early  symptoms  may,  however,  not   be  very  severe.     The 
patient  may  appear  to  progress  favourably  for  a  time,  but 
dyspnoea   and   other   symptoms  of  cardiac  embarrassment 
will  soon  set  in,  for  the  accident  usually  takes  place  at  a 
time  in  life  when    degenerative   changes   are   already  be- 
ginning to  take  place  in  the  walls  of  the  heart,  and  it  is 
incapable    of  undergoing   sufficient   hypertrophy    to   com- 
pensate for  the  valvular  lesion.     Hence  the  ultimate  cause 
of  death,  if  the  patient  survives,  is  a  gradual  stasis  of  the 
circulation,    the    premonitory    indications    being    a    rapid 
increase   in   the   size   of  the  liver,  with   dilatation   of  the 
right  ventricle   following  on    that   of  the   left,  and   later 
the  onset  of  oedema  of  the  extremities.     It  may  be  some 
weeks    or    months    after    the     accident    before    the    fatal 
termination  ensues. 


222  HEART  DISEASE. 

Dilatation  of  the  Orifice. — (a)  The  Aortic  Orifice. — The 
aortic  orifice  is  less  liable  to  dilatation  than  the  mitral, 
owing  to  the  strong  fibrous  ring  surrounding  it.  When 
dilatation  does  occur,  it  usually  takes  place  comparatively 
late  in  life  as  a  part  of  a  general  dilatation  of  the  aorta  due 
to  degenerative  changes  in  the  Avails  of  the  vessel  or  its 
orifice :  it  is  therefore  progressive  in  character  and  the 
prognosis  is  unfavourable,  more  especially  as  these  same 
degenerative  changes  may  lead  to  the  production  of 
aneurysm. 

Syphilitic  disease  of  the  aorta,  invading  the  orifice  and 
valves  and  giving  rise  to  incompetence,  carries  with  it  a 
grave  prognosis. 

(b)  The  Mitral  Orifice. — Speaking  generally,  mitral  re- 
gurgitation, established  by  means  of  dilatation  of  the  left 
ventricle,  in  the  young,  or  as  a  result  of  acute  febrile 
conditions  or  anasmia,  is,  under  favourable  conditions, 
curable.  When  it  is  secondary  to  aortic  disease,  the 
prognosis  necessarily  merges  in  that  of  the  primary  lesion. 
When  it  occurs  as  a  result  of  protracted  high  tension  or 
a  kidney  disease,  it  may  be  temporarily  curable  by  suit- 
able treatment,  but  will  be  liable  to  recur. 

In  later  life  and  old  age  it  may  be  gradually  and 
imperceptibly  established  without  any  obvious  cause  for  it, 
and  it  is  difficult  to  diagnose  between  dilatation  of  the 
orifice  and  changes  such  as  gradual  thickening  and  contrac- 
tion of  the  valves.  It  is  in  such  cases,  however,  very 
slowly  progressive,  as  a  rule. 


CHAPTER  XVI. 

PROGNOSIS  CONTINUED — AGE,  SEX,  HEREDITY — EFFECTS  OF 
HIGH  ARTERIAL  TENSION — HABITS  AND  MODE  OF  LIFE 
OF  THE  PATIENT — ANAEMIA  — THE  CIRCUMSTANCES 
UNDER  WHICH  PROGNOSIS  MAY  HAVE  TO  BE  MADE  :  (1) 
IMMEDIATELY  AFTER  ACUTE  ENDOCARDITIS  ;  (2)  WHEN 
THE  VALVULAR  LESION  IS  SLIGHT  AND  HAS  GIVEN  RISE 
TO  NO  STRUCTURAL  CHANGES  IN  THE  HEART  ;  (3)  WHEN 
COMPENSATORY  CHANGES  HAVE  TAKEN  PLACE  BUT  NO 
SYMPTOMS  OF  EMBARRASSMENT  OF  THE  CIRCULATION 
ARE  PRESENT  ;  (4)  WHEN  SYMPTOMS  OF  FAILURE  OF 
COMPENSATION  HAVE  SET  IN;  (5)  IN  ADVANCED 
VALVULAR  DISEASE  WHEN  SEVERE  SYMPTOMS  OF 
CARDIAC   FAILURE   HAVE    SUPERVENED. 

Age. — Little  need  be  said  with  regard  to  age  as  affecting 
the  prognosis  of  heart  disease.  Late  in  life,  degenerative 
processes  are  almost  invariably  in  operation,  and  the  hyper- 
trophy which  is  needed,  in  order  that  the  effects  of  valvular 
affections  may  be  neutralized,  is  established  with  difficulty  ; 
moreover,  compensatory  hypertrophy,  which  has  served  its 
purpose  for  twenty  or  thirty  years,  may  at  the  end  of  this 
time  be  undermined  by  fatty  or  fibroid  degeneration  of 
the  cardiac  walls. 

Childhood. — In  early  childhood,  the  outbreak  of  rheumatic 
endocarditis  is  always  a  matter  of  grave  prognostic  signifi- 
cance :  firstly,  because  it  is  so  frequently  accompanied  by 
pericarditis,  which  may  prove  fatal  at  the  time  of  the  attack 


224  HEART  DISEASE. 

or  leave  the  heart  permanently  hampered  and  disabled  by 
pericardial  adhesions ;  secondly,  because,  even  though  the 
heart  escapes  serious  damage  from  the  first  attack  of  either 
peri-  or  endocarditis,  both  are  extremely  liable  to  recur. 
Further,  it  would  appear  that  when  a  valvular  lesion  of 
some  severity  is  established,  the  heart  cannot  both  answer 
the  demand  for  hypertrophy  and  keep  pace  with  the  active 
growth  of  this  period  of  life,  so  that  the  child  is  liable  to 
remain  small  and  stunted,  with  clubbing  of  the  fingers  and 
toes,  and  to  be  generally  backward  in  development. 

Sex. — It  is  a  remarkable  fact  that  mitral  stenosis  is  very 
much  more  common  in  women  than  in  men.  The  post- 
mortem statistics  previously  referred  to,  show  that  out  of  53 
cases  of  mitral  stenosis,  38  were  in  females,  and  only  15  in 
males,  which  is  approximately  a  proportion  in  accord  with 
the  experience  of  most  observers.  No  satisfactory  explana- 
tion of  this  predominance  has  yet  been  given. 

On  the  other  hand,  aortic  insufficiency  is  more  frequently 
met  with  in  men,  which  again  is  borne  out  by  the  same 
statistics,  as  out  of  36  cases,  30  were  males,  and  only  6 
females.  This  appears  to  be  explained  by  the  occupation 
and  mode  of  life  of  men ;  in  my  own  experience,  however, 
aortic  regurgitation  has  been  much  more  common  in  boys 
than  in  girls  at  a  period  of  life  long  before  the  influence  of 
occupation  would  begin  to  operate. 

When  valvular  disease  has  been  established  in  childhood, 
girls  are,  according  to  my  experience,  more  likely  to  break 
down  at  the  trying  period  of  puberty  than  boys,  and,  speak- 
ing generally,  the  compensatory  changes  in  the  heart 
walls  are  less  perfectly  effected  in  the  female  than  in  the 
male. 

Hereditary  Tendencies.— In  no  class  of  cases  is  it  more 
necessary  to  inquire  into  the  family  history  than  in  diseases 
of  the  heart.  It  is  more  particularly  in  affections  of  the 
muscular  walls  that  a  family  tendency  to  heart  disease  is 


PROGNOSIS  IN  HIGH  TENSION.  225 

seen,  which  may  take  the  form  of  fatty  degeneration, 
or  of  fibroid  change  secondary  to  high  arterial  tension. 
I  have  known  a  family  in  which  three  out  of  four  brothers 
died  suddenly  before  reaching  the  age  of  fifty-five  from 
disease  of  the  heart  or  aorta,  and  other  examples  almost 
equally  striking ;  similar  histories  must  be  known  to  most 
medical  men  of  large  experience.  It  is  not,  however,  only 
a  special  liability  to  structural  degeneration  of  the  heart  at 
a  certain  age  which  is  important.  In  any  valvular  affection, 
and  at  any  stage,  the  constitution  of  the  patient  is  an 
element  in  the  prognosis  which  must  be  kept  in  view.  We 
have  to  take  into  account,  not  simply  the  cardiac  lesion 
and  the  functional  derangement  of  the  circulation  caused 
thereby,  but  also  the  behaviour  of  the  system  under  this 
disturbing  influence  and  its  power  of  endurance,  and  in  a 
short-lived  family  we  cannot  have  the  same  confidence  in  the 
tissues  as  in  a  family  noted  for  longevity.  More  than  once 
in  my  own  experience,  a  prognosis  based  upon  the  state  of 
the  heart  has  been  falsified  through  failure  of  general  con- 
stitutional power. 

Effects  of  High.  Tension  in  the  Circulation.  —  High 
tension  in  the  arterial  system,  frequently  a  hereditary 
condition,  may  in  itself  be  a  cause  of  chronic  valvular 
disease  in  later  life,  as  has  been  already  stated  in  discuss- 
ing the  causes  of  chronic  endocarditis.  It  increases  the 
shock  of  every  closure  of  the  aortic  valves,  and  renders 
necessary  more  powerful  contraction  of  the  left  ventricle  to 
drive  on  the  blood,  and  thus  increases  the  stress  on  the 
mitral  valve  and  its  tendinous  cords.  The  unremitting' 
strain  thus  imposed  on  both  aortic  and  mitral  valves  is 
more  injurious  than  the  occasional  strain  due  to  violent 
muscular  efforts.  Hence,  when  there  is  high  arterial 
tension  in  addition  to  valvular  disease,  it  will  greatly  tend 
to  aggravate  the  mischief  already  effected,  and  will  con- 
tribute a  grave  addition  to  the  unfavourable  elements  of 

Q 


226  HEART  DISEASE. 

prognosis,  unless  carefully  watched  and  relieved  by  diet 
and  treatment. 

Habits  and  Mode  of  Life  of  the  Patient. — These  have  a 
very  important  bearing  on  the  prognosis.  Violent  efforts 
or  sustained  exertion  impose  a  great  strain  on  the  valves 
of  the  heart ;  vicissitudes  of  temperature  tax  its  power  of 
accommodation  to  different  conditions  of  circulation,  while 
unfavourable  hygienic  influences  tend  to  malnutrition  and 
degeneration.  The  man,  therefore,  who  must  labour  with 
his  hands,  who  is  exposed  to  all  weathers,  whose  food  is  of 
inferior  quality  and  sometimes  insufficient  in  quantity,  who 
breathes  impure  air  and  indulges  perhaps  in  strong  drink, 
who  seeks  advice  only  when  he  can  no  longer  toil,  and 
abandons  all  precautions  as  soon  as  he  leaves  the  hospital,  has 
far  less  chance  of  long  life  than  the  man  who  can  seek  advice 
early  and  has  adequate  means  to  carry  it  out.  There  can  be 
little  probability  of  existing  compensation  being  maintained, 
or  of  rejjarative  hypertrophy  being  established  under  such 
circumstances.  The  first  condition  of  recovery  from  the 
effects  of  disease,  the  removal  of  the  cause  which  gives 
rise  to  these  effects,  is  wanting.  Conversely,  protection 
from  adverse  influences  which  have  precipitated  the  access 
of  symptoms,  together  with  rest,  warmth,  good  food,  and 
care,  may  reverse  an  apparently  hopeless  forecast,  as  is  not 
unfrequently  seen  in  the  all  but  miraculous  recoveries 
which  take  place  in  hospitals.  In  the  same  way,  persistence 
in  habits  of  eating  and  drinking,  which  may  lead  to  valvular 
disease,  directly,  by  overloading  the  blood  with  impurities, 
which  give  rise  to  high  arterial  tension,  or  indirectly,  through 
gouty  inflammation,  will  affect  the  prognosis  unfavourably, 
while  obedience  to  rules  of  diet  carefully  laid  down  and 
supervised  as  to  their  effect  will  incline  the  balance  to  the 
opposite  side. 

Anaemia. — Ansemia,  as  is  well  known,  is  very  common 
at  the  period  of  adolescence,  and  especially  in  girls ;  and 


PROGNOSIS  IN  ANEMIC  SUBJECTS.  227 

its  effects  may  be  most  prejudicial.  About  middle  age, 
essential  or  pernicious  anaemia  may  complicate  heart  disease, 
and  in  at  least  two  instances  which  have  come  under  my 
observation,  has  been  the  real  cause  of  death  which  was 
attributed  to  the  state  of  the  heart. 

But,  in  addition  to  primary  anaemia,  a  deterioration  of 
the  blood  is  a  common  and  almost  inevitable  result  of  heart 
disease  when  this  reaches  a  point  at  which  it  begins  to 
affect  the  circulation.  The  slow  movement  of  the  blood 
through  the  systemic  capillaries  and  through  the  lungs, 
whether  due  to  deficient  vis  a  tcrgo,  as  in  aortic  disease,  or 
to  venous  stasis  in  mitral  disease,  prevents  those  active 
changes  from  taking  place  by  means  of  which  the  blood  is 
constantly  purified  and  renewed.  Absorption  of  food,  again, 
will  be  more  or  less  hindered  by  the  languid  movement  of 
the  blood  in  the  gastro-intestinal  mucous  membrane,  and 
by  the  congestion  of  the  liver,  which  result  from  obstruction 
to  the  return  of  blood  to  the  heart. 

Anaemia,  therefore,  existing  at  a  time  when  prognosis  is 
called  for,  and  especially  a  tendency  to  recurring  anaemia, 
is  a  serious  element  in  the  forecast. 

Anaemia,  however  induced,  has  always  a  detrimental 
influence  on  the  heart.  It  may  of  itself,  aided  by  the  high 
arterial  tension  which  often  accompanies  it,  give  rise  to 
dilatation  of  the  left  ventricle  and  leakage  of  the  mitral 
valve ;  it  will,  therefore,  tend  to  aggravate  such  dilatation 
as  has  already  been  produced  by  valvular  disease,  while 
it  will  retard  compensatory  hypertrophy  by  impairing  the 
quality  of  the  nutritive  material  supplied.  It  is  also 
often  attended  with  palpitation  of  the  heart,  and  will 
add  to  the  liability  of  the  valvular  disease  to  this  distress- 
ing and  sometimes  dangerous  symptom. 

Anaemia,  again,  may  of  itself  give  rise  to  oedema,  and  it 
will  precipitate  the  occurrence  of  dropsy  when  a  tendency 
thereto  exists  from  the  nature  of  the  cardiac  lesion. 


228  heart  disease. 

The  Circumstances  and  Conditions  under  which 
a  Prognosis  may  have  to  be  made. 

1.  We  are  frequently  asked,  during  convalescence 
after  acute  endocarditis — sometimes,  indeed,  before  trie 
attack  has  subsided — how  far  the  heart  is  likely  to  be 
ultimately  affected.  This  is  a  question  to  which  no 
prudent  man  will  give  a  definite  reply.  It  is  impossible 
at  this  time  to  appeal  to  the  changes  in  the  walls  and 
cavities  of  the  heart  for  guidance,  as  there  has  been  no 
time  for  their  development.  The  cardiac  murmurs  are  not 
trustworthy  guides,  as  a  systolic  apex  murmur,  or  some- 
times an  aortic  murmur,  which  has  developed  in  the  course 
of  acute  rheumatism,  may  disappear  afterwards.  If,  however, 
aortic  regurgitation  is  actually  established,  the  prognosis 
is  serious,  although  no  definite  opinion  can  be  formed  as 
to  the  probable  rate  of  progress. 

2.  When  the  lesion  is  one  of  old  standing  we  may  have 
an  individual  in  apparent  health  and  vigour,  scarcely  con- 
scious of  any  inconvenience  arising  from  derangement  of 
the  circulation  even  on  exertion,  but  in  whom  the  discovery 
of  a  valvular  murmur  has  been  made.  There  is  no  modifi- 
cation of  the  pulse,  the  murmur  accompanies  and  does  not 
replace  the  sound  with  which  it  is  associated,  and  there  is 
no  marked  hypertrophy  or  dilatation  of  the  heart.  In  such 
a  case  the  valvular  change  is  slight  and  unimportant,  and 
of  present  danger  there  is  none. 

With  regard  to  the  future  of  such  a  patient,  everything 
depends  on  the  question  whether  the  existing  state  of  the 
valves  is  an  old-standing,  permanent  condition  traceable  to 
a  long  past  attack  of  rheumatic  endocarditis,  or  is  just  the 
beginning  of  mischief,  such  as  chronic  valvulitis,  or  atheroma, 
which  will  go  on  increasing.  In  the  former  case  the  patient 
may  live  to  old  age  and  weather  all  storms  of  illness  and 
hardship  ;  in  the  latter,  if  we  take  as  an  illustration  the  most 


PROGNOSIS    WHEN  COMPENSATION  IS  GOOD.  229 

serious  form  of  disease,  aortic  regurgitation,  he  will  probably 
not  live  more  than  four  or  five  years,  though  a  definite 
judgment  as  to  the  course  and  duration  of  the  affection  can 
only  be  formed  after  repeated  and  careful  examination  at 
long  intervals. 

3.  In  another  case,  while  no  symptoms  are  present, 
there  is  hypertrophy  or  dilatation  of  the  heart,  or  both. 
Here  the  presence  of  structural  changes  testifies  to  the 
existence  of  mechanical  difficulty  due  to  obstruction  or 
regurgitation,  and  shows  that  the  valvular  lesion  is  real  : 
there  will  almost  certainly  be  some  corresponding  modifi- 
cation of  the  pulse,  and  although  compensation  has  been 
established,  the  equilibrium  may  be  disturbed  by  causes, 
which  would  have  no  effect  on  the  normal  heart,  and  once 
overthrown  will  not  be  very  easily  restored.  While,  there- 
fore, under  favourable  circumstances,  the  health  may  remain 
unaffected  for  many  years,  an  illness  of  any  kind,  and 
especially  an  attack  of  bronchitis,  may  be  attended  with 
dangerous  disturbance  of  the  circulation. 

In  such  a  case,  again,  it  is  of  the  utmost  consequence 
whether  the  valvular  disease  is  stationary  or  progressive  : 
should  it  be  progressive,  the  prognosis  will  necessarily  be 
grave,  though  much  will  depend  on  the  seat  and  character 
of  the  valvular  lesion.  The  age,  sex,  general  constitutional 
vigour,  and  family  history  must  be  taken  into  account,  as 
also  the  position  in  life  and  habits  of  the  patient. 

4.  In  another  patient,  symptoms  of  embarrassment  of 
the  pulmonary  or  systemic  circulation  are  present,  habitual 
shortness  of  breath  on  slight  exertion,  violent  or  irregular 
action  of  the  heart  on  slight  provocation,  which  does  not 
readily  subside,  pain  or  a  feeling  of  oppression  in  the 
precordial  area,  incipient  oedema  about  the  ankles  and 
perhaps  albuminuria  with  a  thick  deposit  of  pink  or  high- 
coloured  urates  in  the  urine ;  further  evidences  of  im- 
perfect  compensation  are  also  found  in  the  pulse,  in    the 


230  HEART  DISEASE. 

enlargement  of  the  liver  and  fulness  or  pulsation  of  the 
veins  of  the  neck. 

Here  danger  is  never  far  off  and  may  be  imminent, 
though  by  suitable  precautions  it  may  be  guarded  against 
and  warded  off  for  years.  Speaking  generally,  there  is 
less  probability  of  prolonged  life  and  comfort  after  such 
symptoms  have  set  in,  in  aortic  than  in  mitral  disease. 
There  are  more  chances  of  obviating  the  effects  of  obstruc- 
tion by  compensatory  changes  than  of  making  up  for  failure 
of  vis  a  tcrgo.  As  a  rule,  the  earlier  in  the  course  of 
valvular  disease  symptoms  supervene,  the  more  serious  is 
their  significance. 

5.  In  another  case  we  are  called  upon  to  give  a  prognosis 
when  grave  consequences  of  a  valvular  disease  have  already 
been  developed.  The  occurrence  of  these  serious  symptoms 
may  have  taken  place  in  spite  of  compensatory  changes  in 
the  shape  of  hypertrophy  of  the  right  or  left  ventricle  or 
both,  as  the  case  may  be,  or  for  the  want  of  them ;  we 
must  therefore  consider  whether  by  opportunity  for  the 
restoration  or  establishment  of  compensation  and  by  suitable 
treatment  a  working  equilibrium  can  be  attained.  The 
most  important  question  will  be  whether  the  symptoms 
have  been  brought  on  by  any  temporary  or  removable 
cause,  such  as  over-exertion,  exposure,  anxiety,  recent  acute 
illness,  pulmonary  disease  such  as  bronchitis,  antenna,  or 
debility  or  the  like,  or  whether  there  is  no  recognizable 
cause  for  their  appearance.  In  the  latter  case,  the  prognosis 
is  far  more  serious,  as  some  degenerative  change  in  the 
cardiac  walls  or  organic  weakness  of  the  heart  or  system 
generally,  or  possibly  some  further  complication  in  the 
shape  of  adherent  pericardium,  is  to  be  apprehended.  '  A 
working  man  admitted  into  hospital  will  almost  certainly 
recover,  only  however  to  break  down  again  when  he  resumes 
his  occupation,  and  is  again  exposed  to  the  injurious 
influences  which  brought  on  the  symptoms  of  compensatory 


PROGNOSIS  WHEN  COMPENSATION  HAS  BROKEN  DOWN.    231 

failure.  A  patient  in  easy  circumstances  may  by  care 
maintain  for  a  long  time  the  statum  quo,  but  lie  will  not 
easily  retrace  downward  steps  taken  in  spite  of  all  favouring 
conditions.  The  character  of  the  valvular  change  loses  none 
of  its  importance,  the  only  hope  of  prolonged  immunity  from 
further  consequences  of  failing  or  obstructed  circulation  will 
be  the  absence  of  any  tendency  to  aggravation  of  the  lesion 
in  the  valve.  Subject  to  this  the  soundness  of  the  patient's 
organs  and  tissues  and  the  tenacity  of  life  exhibited  by  the 
family  history  will  be  elements  of  great  consequence. 

6.  When  we  are  called  upon  to  form  an  opinion  of  the 
chances  of  recovery  of  a  patient  who  is  suffering  from 
advanced  dropsy,  with  severe  pulmonary  congestion  and 
extreme  dyspnoea,  then  indeed  the  stationary  or  progressive 
character  of  the  lesion  has  no  longer  any  bearing  on  the 
immediate  issue  of  the  case.  If  the  symptoms  have  been 
gradually  increasing  in  severity  without  any  apparent  cause, 
and  the  dropsy  has  crept  on  from  the  legs  and  invaded 
the  trunk,  and  the  dyspnoea  is  extreme  even  while  the 
patient  is  at  rest  in  bed,  then  there  is  little  hope  of  recovery. 
If,  on  the  other  hand,  the  access  of  severe  symptoms  is 
traceable  to  over-exertion  or  a  chill  or  intercurrent  pulmo- 
nary trouble,  such  as  bronchitis,  then  there  is  a  hope  that 
suitable  treatment  may  for  a  time  restore  the  compensatory 
balance,  provided  that  there  is  evidence  of  a  certain  degree 
of  vigour  and  force  in  the  cardiac  impulse,  more  especially 
in  that  of  the  right  ventricle.  If  it  is  a  second  attack  of 
this  kind,  there  will  be  less  chance  of  recovery,  and  any 
complication,  such  as  kidney  disease,  will  diminish  mate- 
rially this  chance.  The  occurrence  of  a  pulmonary  apoplexy 
at  this  stage,  or  of  thrombosis  of  the  veins  of  the  leg,  will 
be  of  very  serious  import,  rendering  the  prognosis  as  regards 
the  prolongation  of  life,  even  for  a  short  period,  almost 
hopeless. 


CHAPTER  XVII. 
TREATMENT   (GENERAL). 

TREATMENT  OF  VALVULAR  DISEASE  IN  GENERAL — PROPHY- 
LACTIC MEASURES — GENERAL  RULES,  IN  CASES  WHERE 
LESION  IS  NOT  OP  SERIOUS  EXTENT,  AS  TO  EXERCISE, 
CERTEL  AND  SCHOTT  TREATMENTS,  CLIMATE,  CHOICE  OF 
RESIDENCE,  DIET,  STIMULANTS  —  TREATMENT  WHERE 
LESION  IS  OF  MORE  SERIOUS  NATURE  AND  HAS  GIVEN 
RISE  TO  MARKED  HYPERTROPHY  AND  DILATATION  OF 
THE  HEART — PRECAUTIONS  TO  BE  TAKEN — SELECTION 
OF  WINTER  RESORT — REST  IN  BED— DIET— STIMULANTS 
— EMPLOYMENT  OF  DRUGS— TREATMENT  OF  VENOUS 
CONGESTION  —  VENESECTION  —  TREATMENT  IN  AORTIC 
DISEASE. 

The  treatment  of  valvular  disease  of  the  heart  has  been 
foreshadowed  in  the  consideration  of  its  prognosis.  What- 
ever influences  have  been  seen  to  affect  unfavourably  the 
condition  of  the  circulation  and  of  the  patient,  such  must 
be  averted  or  counteracted,  and  injurious  tendencies  arising 
out  of  the  particular  lesions  of  the  valves  must  be  combated. 
The  order  also  in  which  the  therapeutic  methods  and 
resources  employed  for  the  above  ends  must  be  discussed  is 
dictated  by  the  arrangement  adopted  in  the  consideration 
of  the  prognosis. 

One  of  the  most  important  prophylactic  measures  is  the 
prevention,  as  far  as  possible,  of  the  ill  effects  on  the  heart 
of  a  recently  established  valvular  lesion.  When  an  attack  of 
endocarditis  has  subsided,  leaving  behind  it  some  valvular 
lesion,  the  exercise  of  caution  and  care  will  prevent  undue 


TREATMENT  OF   VALVULAR  DLSEASE.  233 

cardiac  dilatation,  which  might  prove  rapidly  fatal  or 
cripple  the  heart  seriously  in  the  future. 

The  patient  should  be  kept  in  bed,  or  confined  to  his 
room  for  some  weeks,  or  perhaps  even  months,  according 
to  the  degree  of  severity  of  the  lesion,  cases  of  aortic 
incompetence  requiring  the  longest  period  of  rest.  The 
object  of  protracted  rest  is  to  allow  time  for  the  necessary 
compensatory  hypertrophy  of  the  cardiac  walls  to  take 
place.  In  many  cases,  more  especially  when  pericarditis 
accompanies  the  endocarditis,  as  it  frequently  does  in 
children,  the  heart  is  left  dilated  and  weakened  after  the 
subsidence  of  the  attack,  so  that  the  risk  from  premature 
exertion  will  be  doubly  serious,  and  the  period  of  rest 
required  afterwards  will  be  proportionately  longer. 

In  children,  in  whom  the  joint  manifestations  of  rheu- 
matism are  usually  slight,  while  the  heart  is  frequently 
attacked,  the  heart  should  be  examined  from  time  to  time 
if  there  is  the  slightest  suspicion  of  rheumatism,  such  as 
fugitive  pains  in  the  joints  or  limbs,  with  rise  of  tempera- 
ture, still  more  if  there  are  obvious  manifestations  such  as 
rheumatic  nodules ;  for  the  onset  of  pericarditis  or  endo- 
carditis is  often  very  insidious,  and  serious  mischief  may 
result  before  it  is  detected,  if  the  child  is  allowed  to  go 
about  as  usual. 

When  the  lesion  is  established,  and  sufficient  rest  after 
the  attack  of  endocarditis  has  been  allowed,  the  next 
question  to  be  settled  will  be,  how  far  the  patient  may  live 
his  ordinary  life,  or  what  rules  must  be  laid  down  for  his 
future  conduct,  and  what  precautions  should  be  taken. 
Everything  will  of  course  depend  on  the  nature  and  the 
degree  of  severity  of  the  lesion,  and  in  discussing  the  treat- 
ment the  less  severe  class  of  cases  will  be  first  considered, 
in  which  there  is  no  evidence  in  the  shape  of  marked  cardiac 
dilatation  or  hypertrophy  that  the  lesion  is  considerable. 

Exercise. — Almost   the  first  question  will  be  as  to  the 


234  HEART  DISEASE. 

rules  to  be  laid  down  with  regard  to  exercise  and  exposure 
to  changes  of  temperature.  These  will  necessarily  vary 
according  to  the  character  and  seat  of  the  lesion,  but  not 
so  only — the  constitution,  strength,  habits,  and  disposition 
of  the  patient  will  also  have  to  be  considered.  One  man 
is  timid  and  apprehensive ;  he  will  scarcely  move  out  of 
doors  lest  he  should  overtax  his  heart,  or  eat  a  sufficient 
meal  for  fear  of  palpitation,  or  go  away  for  change  of  air 
lest  he  should  die  away  from  home.  He  must  be  encouraged 
or  even  compelled  to  take  exercise.  Another  is  only  too 
ready  to  ignore  the  state  of  his  heart,  and  will  run  or  row 
or  swim  or  take  part  in  violent  games ;  he  must  be  warned 
against  imprudence,  and  it  may  be  necessary  to  forbid  such 
forms  of  exertion  as  are  liable  to  be  indulged  in  to  excess. 
In  another,  an  eager  temperament  and  impetuous  disposition 
may  reside  in  a  weakly  frame,  and  ordinary  duties  and  an 
average  amount  of  work  may  be  done  with  injurious  energy 
and  haste.  It  is  not  possible,  therefore,  to  draw  up  definite 
regulations  applicable  to  all  cases.  To  make  the  restrictions 
imposed  too  severe  will  in  one  person  directly  injure  the 
sufferer's  health;  in  another,  will  make  him  unnecessarily 
depressed  and  miserable ;  in  a  third,  will  provoke  revolt  and 
lead  to  rash  and  dangerous  violation  of  all  rules.  The 
principle  on  which  recommendations  must  be  based  will  be 
to  interfere  as  little  as  possible  with  the  avocation,  habits, 
and  mode  of  life  of  the  patient,  as  long  as  these  are  not 
injurious,  and  especially  to  allow  a  maximum  of  exercise 
in  fresh  air  compatible  with  safety. 

Nothing  can  be  worse  than  to  debar  all  patients  who 
are  found  to  have  valvular  disease  from  games  and  vigorous 
exercise,  and  to  forbid  them  to  go  upstairs  or  to  walk 
uphill,  and  on  no  cases  do  I  look  back  with  greater  satis- 
faction than  on  those,  and  they  have  not  been  few,  in  which 
I  have  liberated  boys  and  girls  from  such  orders.  In  the 
class   of  cases   under  consideration,  supposing  a  sufficient 


THE    CERTEL    TREATMENT.  235 

time  to  have  elapsed  after  the  acute  attack  in  which  the 
valvular  affection  was  established  for  the  necessary 
compensatory  changes  to  take  place,  a  girl  may  be  allowed 
to  take  long  walks,  to  play  lawn  tennis,  to  ride,  cycle, 
swim,  and  dance,  and  a  boy  to  play  cricket  and  racquets, 
to  hunt,  box,  and  fence,  provided  that  these  exercises  are 
not  attended  with  undue  breathlessness  and  distress,  and 
that  they  are  entered  upon  gradually  and  practised  with 
moderation  and  discretion.  On  the  other  hand,  football, 
paper-chases,  long  house-runs,  training  for  races  of  any 
kind,  are  scarcely  permissible. 

While  discussing  the  question  of  exercise  the  (Ertel 
and  Schott  methods  may  be  described. 

The  (Ertel  Treatment  consists  in  systematic,  graduated 
muscular  exercise  carried  out  at  a  certain  elevation,  about 
two  thousand  feet  above  sea-level.  The  patient  is  required 
to  walk  a  certain  distance  up  a  gentle  ascent  each  day,  the 
distance  and  pace  being  gradually  increased.  At  the  same 
time  the  diet  is  carefully  regulated,  and  the  amount  of 
fluids  ingested  is  strictly  limited.  The  object  of  the  treat- 
ment is :  firstly,  to  stimulate  the  heart  by  muscular  exercise, 
carefully  adjusted  to  the  capacity  of  the  patient,  so  as  to 
bring  about  hypertrophy  of  its  walls ;  secondly,  to  diminish 
the  volume  of  blood  in  circulation  by  restricting  the  amount 
of  water  consumed,  and  increasing  the  amount  eliminated. 
(Ertel  claims  that  this  treatment  is  successful  in  cases  of 
fatty  heart  uncomplicated  by  disease  of  the  coronary  arteries, 
in  cardiac  dilatation,  and  in  valvular  disease,  even  when 
compensation  has  broken  down,  and  dropsy  with  other 
evidence  of  venous  congestion  is  present. 

In  cases  of  valvular  disease,  in  which  compensation  has 
completely  given  way,  this  treatment  is  certainly  not 
advisable,  nor  in  many  instances  would  it  be  possible ;  but 
where  compensation  has  been  established  after  a  recent 
valvular  lesion,  or  has  been  restored  by  rest  and  suitable 


236  HEART  DISEASE. 

treatment,  or  where  it  is  maintained  with  some  difficulty, 
gentle  climbing  exercise  in  fresh  and  pure  and  somewhat 
rarefied  air  will  certainly  do  more  to  develop  further  com- 
pensatory hypertrophy  of  the  heart,  than  mere  walking  on 
the  level,  which  has  not  the  same  beneficial  effect  on  the 
circulation,  and  where  the  air  is  not  so  pure  or  invigorating. 

It  is  more  especially  in  cases  of  fatty  infiltration  of  the 
heart  without  fatty  degeneration  of  the  cardiac  muscle, 
arising  from  overeating  and  drinking  and  insufficient 
exercise,  that  this  treatment  by  dieting  and  systematic 
muscular  exercise  may  be  of  real  service.  At  the  com- 
mencement of  the  treatment,  great  caution  should  be 
observed  as  to  the  nature  and  amount  of  exercise.  The 
patient  should  only  be  allowed  to  walk  a  certain  distance 
up  a  gentle  slope,  and  each  day  the  distance  may  be 
gradually  increased.  By  this  means,  and  by  the  limitation 
of  the  fluids  ingested,  the  superfluous  adipose  tissue  is 
gradually  got  rid  of,  and  the  tone  of  the  heart  muscle  is 
restored.  Not  infrequently  this  treatment  is  employed  as 
a  sequel  to  the  Nauheim  methods. 

The  Schott  Treatment. — The  treatment  by  baths  and 
exercises  by  the  method  of  Schott,  of  Nauheim,  may  be 
of  service  in  suitable  cases.  The  waters  of  Nauheim 
are  remarkably  rich  in  free  carbonic  acid  gas,  as  well  as 
in  mineral  constituents,  the  chief  of  which  are  chloride 
of  sodium,  and  chloride  of  calcium,  and  carbonate  of  iron. 
At  the  beginning  of  the  treatment  the  baths  should 
contain  about  1  per  cent,  of  chloride  of  sodium,  and 
1  per  1000  of  calcium  chloride,  and  should  be  free  from 
carbonic  acid  gas.  The  bath  at  first  should  last  from  six 
to  eight  minutes,  and  should  be  of  the  temperature  of 
92°  to  95°  Fahr.  As  time  goes  on  the  proportion  of 
solids  in  the  bath  should  be  increased,  also  the  duration 
of  the  bath,  while  the  temperature  is  gradually  lowered. 
Eventually,  baths  containing  free  carbonic  acid  gas,  and 


THE  SCHOTT  TREATMENT.  237 

about  3  per  cent,  of  sodium  chloride  and  3  per  1000  of 
calcium  chloride,  may  be  taken.  Baths  can  be  artificially 
prepared  in  imitation  of  those  at  Nauheini,  the  essential 
ingredients  being  the  chlorides  of  sodium  and  calcium 
and  the  free  carbonic  acid  gas. 

The  exercises  consist  of  a  series  of  simple  movements  of 
each  limb  and  of  the  trunk  made  against  slight  resistance, 
so  that  every  muscle  of  the  body,  as  far  as  possible,  is  in 
turn  brought  into  play.  The  movements  should  be  made 
slowly  and  systematically,  and  a  short  interval  of  rest  should 
be  interposed  between  each ;  they  should  be  stopped  if  the 
patient  experiences  any  distress  in  breathing  or  discomfort, 
but  may  be  proceeded  with  again  as  soon  as  he  is  rested. 
The  movements  consist  of  flexions,  extensions,  adductions, 
abductions,  and  rotations  of  each  limb  in  turn,  and  of 
flexion,  extension,  and  rotation  of  the  trunk. 

The  effects  produced  on  the  circulation  and  the  heart, 
whether  by  the  baths  or  exercises,  are  similar ;  the  pulse 
frequency  is  diminished,  its  volume  and  force  are  increased, 
and  the  area  of  cardiac  dulness  in  cases  of  cardiac  dilata- 
tion is  diminished,  while  the  apex  beat  recedes  and  comes 
nearer  to  the  normal  position. 

Such  are  the  immediate  results  which  appear  to  indicate 
an  improvement  in  the  contractile  power  of  the  heart  and 
a  reduction  of  its  dilatation ;  but  these  are  not  permanent. 

Similar  temporary  results  may,  indeed,  be  obtained  in  a 
normal  individual  as  the  immediate  effect  of  a  simple  hot 
or  cold  bath  without  any  saline  constituents. 

Too  much  importance  is  attached  by  advocates  of  the 
Schott  treatment  to  the  percussing  out  of  the  area  of 
cardiac  dulness  and  to  the  diminution  it  is  said  to  undergo 
after  each  bath,  more  especially  when  the  so-called 
auscultatory  method  is  employed.  This  method  lends 
itself  very  much  to  the  imagination,  and  is  absolutely 
untrustworthy.     A  shifting  inwards  of  the  apex  beat  is  of 


238  HEART  DISEASE. 

importance,  but  in  cases  of  dilatation  from  over-exertion 
a  similar  inward  movement  of  the  apex  may  sometimes 
be  effected  by  making  the  patient  walk  rapidly  two  or 
three  times  across  the  room.  It  is  also  probable  that  the 
diminution  of  percussion  dulness  is  due,  not  so  much  to 
fluctuations  in  the  size  of  the  heart  as  to  encroachment  by 
the  lungs  on  the  cardiac  area,  due  to  deeper  respirations 
taken  while  the  patient  is  in  the  bath.  It  does  not  there- 
fore follow  that,  because  the  area  of  cardiac  dulness  diminishes 
after  a  bath,  the  heart  was  previously  dilated.  Moreover, 
accurate  delineation  of  the  outline  of  the  heart  by  per- 
cussion is  in  many  cases  impossible,  and  even  in  the  mere 
percussing  out  of  the  area  of  superficial  cardiac  dulness 
there  may  be  many  difficulties  and  sources  of  error  in  the 
adult,  from  the  solid  nature  of  the  chest  walls  and  the 
thickness  of  their  coverings,  from  an  emphysematous  con- 
dition of  the  lungs,  or  from  pleuro-pericardial  adhesions. 
It  is  difficult,  therefore,  to  attach  any  real  value  to  the 
remarkable  diagrams  of  the  cardiac  dulness  "  before  "  and 
"  after  "  the  bath,  published  in  quantity  by  the  enthusiastic 
advocates  of  this  treatment,  and  one  is  compelled  to 
question  their  accuracy  if  not  their  honesty.  Even  if  they 
approximate  the  truth,  they  are  worth  nothing  if  there  is 
not  other  evidence  of  improvement  in  the  general  condition 
of  the  patient  and  in  the  symptoms  and  physical  signs  of 
the  affection  from  which  he  is  suffering.  The  treatment 
cannot,  of  course,  cure  a  valvular  lesion,  but  it  may  give 
beneficial  results  in  suitable  cases.  But  it  is  rather  in 
cases  of  cardiac  dilatation  from  loss  of  tone  after  influenza, 
or  some  depressing  disease,  and  in  cases  of  functional 
and  neurotic  heart  disease,  than  in  actual  valvular  disease, 
that  it  is  satisfactory.  The  change  of  air  and  scene,  the 
sedative  effect  of  the  baths,  the  enjoined  rest  after  each 
bath,  the  quiet,  uneventful  life,  the  early  hours  and  regular 
meals,  together  with  freedom  from  excitement  and  worry, 


GENERAL  HYGIENIC   TREATMENT.  239 

and  the  satisfaction  engendered  by  "  taking  a  cure,"  will 
be  among  the  most  important  factors  which  contribute  to 
its  success  in  this  class  of  cases. 

Exposure  to  Change  of  Temperature. — As  regards  exposure 
to  vicissitudes  of  temperature  and  to  changes  of  weather, 
we  have  to  bear  in  mind  that  the  subjects  of  valvular 
disease  have,  in  most  cases,  already  manifested  a  suscepti- 
bility to  the  effects  of  cold  and  wet,  or  an  inherited 
predisposition  to  rheumatism.  One  of  the  things,  therefore, 
most  to  be  feared  and  guarded  against,  is  another  attack  of 
rheumatism.  Flannel  or  woollen  underclothing  of  some 
kind  should  be  worn  next  to  the  skin  winter  and  summer, 
and  standing  or  sitting  with  wet  feet  or  in  damp  clothes,  or 
lying  down  on  the  grass  after  games,  involving  the  risk  of 
getting  chilled  after  perspiration,  must  be  forbidden.  But 
we  must  not  go  to  the  other  extreme  and  cultivate  an  undue 
susceptibility  to  cold  by  excessive  care.  The  patient  need 
not  be  kept  indoors  by  rain  or  cold,  or  forbidden  to  get  into 
a  perspiration.  Excessive  precautions  defeat  the  object  for 
which  they  were  enjoined,  and  it  is  easy  to  reduce  the 
power  of  resistance  to  changes  of  temperature  until  the 
slightest  exposure  is  attended  with  risk.  While,  however, 
the  primary  aim  ought  to  be  to  maintain  and  confirm  such 
hardihood  as  the  constitution  possesses  or  is  capable  of, 
there  are  cases  in  which  safety  consists  in  flight  from  too 
severe  a  climate,  or  from  a  situation  or  soil  conducive  to 
rheumatism.  There  is  full  opportunity  for  the  exercise  of 
judgment  in  deciding  how  much  may  be  dared  and  how 
soon  the  patient  must  yield. 

Climate. — Climate  may  do  much  to  influence  the  course 
of  heart  disease.  On  a  priori  grounds,  we  should  say  that  a 
mild,  dry,  bracing  and  equable  climate,  in  which  the  patient 
could  have  a  maximum  of  exercise  in  the  open  air,  would  be 
the  best ;  but,  independently  of  the  question  where  these 
desiderata  are  to  be  found,  all  such  general  statements  have 


240  HEART  DISEASE. 

to  be  qualified  to  meet  the  idiosyncrasies  of  individuals ; 
the  great  majority  of  our  patients,  moreover,  are  tied  down 
by  circumstances  to  a  particular  spot,  and  the  most  important 
practical  problem  usually  is  how  to  make  the  best  of  a  given 
neighbourhood. 

Choice  of  Residence. — If  the  choice  of  a  residence  is  open 
we  should  direct  the  patient  to  seek  a  gravelly  or  sandy 
soil  at  a  moderate  elevation,  where  the  rainfall  is  below  and 
the  sunshine  above  the  average,  and  the  water  not  hard ; 
conditions  best  realized — in  England — in  Kent,  Surrey,  and 
Sussex.  The  exposure  of  the  house  should  be  to  the  south, 
and  there  should  be  protection  from  the  north  and  east. 
The  immediately  surrounding  country  should  not  be  too 
hilly,  and  especially  the  house  itself  should  not  be  on 
the  top  of  a  steep  hill,  making  every  walk  necessarily  end 
in  an  ascent.  There  would  be  danger,  some  day  or  other, 
of  dilatation  or  other  ill  effect  from  the  exertion  after  a 
longer  or  more  tiring  walk  than  usual  or  when  out  of  sorts. 
It  must  always  be  borne  in  mind  that  the  good  results 
obtainable  from  the  best  climate  may  be  neutralized  by 
faults  of  detail  in  the  placing  or  construction  of  a  house. 

Diet.— About  food  little  need  be  said.  Excess  should 
be  avoided,  but,  subject  to  this  condition,  the  diet  may  be 
liberal  and  varied.  It  is  important,  however,  that  there 
should  be  a  due  proportion  of  farinaceous  and  vegetable 
articles  of  diet;  when  the  food  is  highly  nitrogenized,  as 
when  it  consists  largely  of  meat,  imperfectly  oxidized  waste 
accumulates  in  the  blood,  and  this  is  a  great  cause  of 
resistance  in  the  capillary  circulation,  which  constitutes  a 
serious  addition  to  the  work  imposed  upon  the  heart,  and 
puts  a  continued  strain  upon  the  compensation  by  which  it 
adjusts  itself  to  the  imperfect  state  of  the  valves.  This 
recommendation  is  specially  important  in  the  case  of 
constitutions  disposed  to  gout,  since  the  valves  may  be 
further  damaged  by  gouty  inflammation.     Habitual  excess 


GENERAL  HYGIENIC   TREATMENT.  241 

of  food  beyond  the  requirements  of  the  system  will  have 
the  same  effect. 

The  food,  again,  should  be  divided  into  three  fairly 
equal  meals,  and  not  taken  in  excessive  quantity  at  dinner, 
or  at  breakfast  and  dinner.  If  the  nourishment  for  the 
twenty-four  hours  is  consumed  at  one  huge  repast,  the  blood, 
in  the  long  interval,  is  drawn  upon  for  the  nutrition  of 
the  tissues  and  for  the  supply  of  the  secretions  and  its 
volume  being  reduced,  the  vessels  are  depleted;  the 
products  of  digestion  are  then  rapidly  absorbed,  the  amount 
of  blood  is  increased,  and  the  vascular  system  is  rapidly 
filled  and  perhaps  overcharged.  Wide  variations  in  the 
volume  and  pressure  of  the  blood  are  thus  liable  to  result, 
and  are  harmful  to  the  patient. 

When  its  valvular  apparatus  is  unsound,  or  its  structure 
is  impaired,  the  heart  does  not  easily  adjust  itself  to  such 
extremes,  and,  if  it  so  far  effects  this  that  no  particular 
discomfort  is  experienced,  the  increased  work  thrown  upon 
a  weak  organ  cannot  fail  to  be  injurious  in  the  long  run. 
A  very  large  meal,  again,  must  distend  the  stomach,  and  the 
diaphragm  may  be  pushed  up  and  hindered  in  its  action  so 
as  to  embarrass  the  heart  directly  by  pressure,  and  indirectly 
by  interference  with  respiration.  A  dilated  stomach  by 
upward  pressure  may  so  embarrass  a  heart  which  is  dis- 
eased as  to  give  rise  to  irregularity  of  rhythm,  anginoid 
pains,  and  even  syncopal  attacks,  one  of  which  may  prove 
fatal. 

Stimulants. — Strict  moderation  must  be  observed  in  the 
matter  of  alcoholic  drinks ;  in  comparatively  few  cases  are 
they  necessary,  and  if  taken  they  should  be  taken  only  as 
part  of  a  substantial  meal.  Their  effects  as  excitants  of  the 
heart  may,  to  some  extent,  be  neutralized  by  the  relaxation 
of  the  peripheral  vessels  which  they  induce,  but  their  general 
tendency  is  to  interfere  with  due  metabolism  and  elimina- 
tion, and  to  bring  about  degeneration  of  structure. 

R 


242  HEART  DISEASE. 

Unduly  high  arterial  tension,  from  whatever  cause,  must 
be  combated.  Its  injurious  effects  have  been  already  pointed 
out.  The  regulations  as  to  diet  and  drink  have  for  one  of 
their  objects  the  prevention  of  high  blood-pressure.  When 
this  condition  exists  from  inherited  tendency,  or  from  gout 
or  renal  disease,  it  must  be  kept  down  within  safe  limits  by 
suitable  eliminants. 

Regulation  of  Bowels. — It  is  always  important  to  take 
measures  against  constipation.  Accumulation  of  fsecal 
matters  in  the  large  intestine,  with  the  associated  flatulent 
distension,  will  more  or  less  embarrass  the  heart,  both  by 
direct  pressure  upwards  of  the  diaphragm  and  indirectly  by 
interference  with  respiratory  movements.  Palpitation,  again, 
is  a  frequent  result  of  constipation,  and  both  the  effort 
required  to  unload  the  bowel  and  the  different  pressure  on 
the  abdominal  veins  before  and  after  a  large  evacuation  put 
stress  upon  the  heart.  A  further  ill-result  is  the  retention 
of  toxic  matters  in  the  blood,  which  provoke  resistance 
in  the  capillaries  and  tend  to  the  production  of  high 
tension. 

Anaemia. — While  everything  is  done  to  maintain  the 
general  health,  special  precautions  must  be  taken  to  guard 
against  anaemia.  We  have  seen  that  it  may  itself  give  rise 
to  dilatation  of  the  left  ventricle,  which  is  a  most  serious 
aggravation  of  valvular  disease.  Valvular  disease,  moreover, 
tends  to  deteriorate  the  blood  in  so  far  as  it  interferes  with 
its  free  movement  through  the  glands  and  tissues  generally, 
and  to  produce  antenna.  It  does  not  follow  that  we  are  to  be 
always  giving  iron  or  other  reconstituent  tonics,  but  it  is  a 
valid  reason  for  careful  choice  of  residence  and  for  frequent 
change  of  air,  and  for  attention  to  and  treatment  of  the 
earliest  indications  of  anaemia. 


regulation  of  exercise.  243 

Treatment  in  Cases  of  Severe  Valvular  Lesion. 

When  the  presence  of  dilatation  and  hypertrophy  in- 
dicate that  the  damage  to  the  valve  has  been  such  as  to 
interfere  perceptibly  with  transmission  of  the  blood  through 
the  heart,  while  the  principles  with  regard  to  exercise  remain 
the  same,  some  modification  in  their  application  will  be 
necessitated.  Each  form  of  valvular  disease  gives  rise  to  a 
certain  kind  and  degree  of  interference  with  the  efficient 
pumping  of  the  blood  through  the  heart,  lungs,  and  system, 
which  tends  to  the  production  of  results  injurious  to  health, 
and  in  the  long  run  dangerous  to  life.  We  must  not  Avait 
for  the  recognition  of  such  tendencies  till  they  are  forced 
upon  our  attention  by  the  appearance  of  symptoms  ;  they 
can  always  be  foreseen,  and  they  may  often  be  prevented. 
Again,  it  must  be  borne  in  mind  that  when  valvular  disease 
of  any  importance,  as  indicated  by  changes  in  the  walls  and 
cavities,  exists,  the  heart  has  to  some  extent  lost  the  power 
of  responding  to  sudden  calls  for  variations  in  the  rate  or 
force  of  the  circulation ;  more  than  this,  its  power  of  re- 
covering itself  after  disturbance  is  impaired.  The  com- 
pensation effected  by  hypertrophy  is  efficient  only  for 
ordinary  purposes,  or  within  certain  limits  more  or  less  re- 
stricted. When  the  muscular  pressure  on  the  veins  all  over 
the  body,  which  attends  vigorous  exercise,  brings  the  blood 
in  increased  quantity  to  the  right  cavities  of  the  heart,  it 
cannot  be  sent  on  against  the  resistance  in  the  pulmonary 
circulation,  which  results,  as  we  have  seen,  from  most  forms 
of  valvular  disease.  Even  in  health  there  is  a  period  of 
breathlessness  before  the  right  ventricle  succeeds  in  driving 
the  blood  through  the  lungs  as  fast  as  it  arrives  from  the 
system,  when  we  begin  to  run,  and  in  disease,  this  breath- 
lessness is  more  readily  provoked  and  is  easily  exag- 
gerated to  painful  dyspnoea ;  the  distended  condition  of 
the    right    ventricle    and    auricle,    which  is    induced    by 


244  HEART  DISEASE. 

exertion  in  health,  and  which  acts  as  a  reservoir  for  the 
blood  till  it  can  be  delivered  to  the  lungs  by  the  increased 
action  of  the  heart,  may  already  exist  in  disease,  so  that 
the  provision  for  the  emergency  is  already  exhausted,  and 
there  is  no  margin  left  for  severe  exertion. 

While,  therefore,  we  avoid   unnecessary  and   injurious 
restrictions  on  exercise,  sudden  and  violent  exertions  must 
be   forbidden,  and   it   must  be   understood   that   anything 
which  gives  rise  to  painful  breathlessness  is  injurious.     A 
patient,  however,  will  often,  by  beginning  gradually,  arrive 
at  a  rate  of  walking  which  attempted  at  first  would  have 
been  impossible,  and  may  eventually,  by  the  exercise  of 
similar  caution,  mount  with  ease  an  incline  which  would 
otherwise  have  brought  him  to  a  standstill.     So  long  as  the 
equilibrium  of  the  circulation  is  not  disturbed,  there  is  no 
particular  danger  in  going  uphill.     The  danger  arises  from 
the  fact  that  on  coming  to  an  ascent,  the  tendency  is  to 
maintain  the  same  pace  as  on  level  ground  until  we  are 
checked  by  shortness  of  breath.     The  sufferer  from  heart 
disease  cannot  afford  to  do  this.     What  would  be  a  mere 
fugitive  inconvenience  to  a  man  in  health  may  be  a  risk 
and  injury  to  him.     If,  however,  he  will  exercise  a  little 
foresight  and  slacken  his  pace  immediately  on  coming  to  an 
incline,  he  may  afterwards  gradually  increase  it  again  within 
certain  limits  and  so  climb  hills.  The  same  conclusions  apply 
to  stairs.    So  long  as  the  subject  of  a  valvular  affection 
can  go  upstairs  quite  comfortably,  there  is  no  objection 
to   his   doing  so ;   and   if  by  ascending  them  quietly  he 
avoids  breathlessness,  this  need  not  be  forbidden  even  when 
symptoms  are  already  manifest.    Sometimes  he  can  go  up 
backwards  without  distress,  when  to  take  them  step  by  step  in 
the  ordinary  way  is  difficult.     But  there  comes  a  time  when 
stairs  must  be  avoided  as  far  as   possible,   and   when   the 
patient  must  be  carried  up  or  must  live  on  one  floor.    This 
will  especially  be  the  case  when   not  mere  breathlessness 


SELECTION  OF   WINTER  RESORT.  245 

but  faintness  is  produced  by  slight  exertion,  and  the  patient 
feels  giddy  or  has  dimness  or  temporary  loss  of  vision,  or 
weakness  and  trembling  of  the  knees  after  going  uphill  or 
upstairs.  It  is  in  aortic  disease  that  such  symptoms  are 
most  likely  to  be  experienced,  but  they  may  occur  whenever 
the  left  ventricle  is  greatly  dilated  or  is  weak  from  any 
cause. 

Age.— In  applying  any  rules  for  the  management  of 
valvular  disease  of  the  heart,  a  great  difference  will  be  made 
between  the  young  and  those  who  have  reached  or  passed 
middle  age.  After  a  certain  period  of  life,  varying  greatly 
according  to  constitution  and  habits,  there  is  a  liability  to 
dilatation  of  the  heart  on  exertion,  and  this  condition, 
attended  at  once  by  symptoms  and  leading  to  a  speedy 
fatal  issue,  is  often  brought  about  by  an  imprudent  effort 
independently  of  any  pre-existing  affection  of  the  valves. 
The  risk  of  such  an  event  is  indefinitely  increased  when 
dilatation,  attendant  on  valvular  lesion,  is  already  present  ; 
or  when  the  tendency  thereto  has  only  been  neutralized 
by  compensatory  hypertrophy.  The  ventricle  is  tried  by 
chronic  overwork,  and  the  nutrition  of  the  increased  amount 
of  muscular  tissue  in  the  walls  is  maintained  with  difficulty, 
the  heart  is  consequently  more  ready  to  break  down  under 
stress.  We  may,  therefore,  allow  a  boy  to  play  cricket,  or 
the  young  of  either  sex  to  play  lawn  tennis,  to  boat,  or 
even  swim  in  moderation,  provided  always  that  no  distress 
of  breathing  or  tendency  to  syncope  is  induced,  while  a 
corresponding  amount  of  exertion  would  be  altogether  for- 
bidden at  middle  age. 

Under  no  circumstances,  and  at  no  age,  must  fatigue  be 
carried  to  the  point  of  exhaustion.  There  is  less  chance  of 
recovery  from  the  effects  of  overtaxed  endurance  than  from 
those  of  a  brief  violent  effort. 

Selection  of  Wintering  or  Holiday  Place. — In  deciding  upon 
a  place  for  temporary  change  of  air  for  a  patient  suffering 


246  HEART  DISEASE. 

from  valvular  disease,  we  must  be  guided  very  much  by  the 
previous  experience  of  the  patient.  In  some  cases  a  trip  by 
sea  will  be  of  the  greatest  service,  but  this  could  be  recom- 
mended only  to  good  sailors.  A  winter  in  Egypt,  Algiers, 
or  Rome  may  be  good  in  others,  or,  if  this  is  not  practicable, 
a  few  months  on  the  south  coast  of  England,  at  places 
where  exercise  can  be  taken  without  much  up  and  downhill. 
In  summer  the  seaside  is  most  generally  useful ;  but  some 
people  tell  us  it  does  not  suit  them,  that  it  makes  them 
bilious.  This  is  often  a  mere  temporary  effect,  which  quickly 
passes  off,  or  it  may  be  a  result  of  the  constipation,  which 
is  common.  In  all  cases  constipation  must  be  provided 
against. 

When  change  of  air  is  recommended,  great  caution  must 
be  exercised  in  sending  patients  suffering  from  heart  disease 
to  any  considerable  height,  such  as  5000  or  6000  feet.  The 
effects  of  the  reduction  of  atmospheric  pressure  cannot  be 
foreseen ;  paljDitation  is  often  set  up  which  is  absolutely 
intractable  without  removal  to  a  lower  level,  and  this  is 
sometimes  difficult.  One  reason  for  this  may  possibly  be 
the  expansion  of  the  gases  in  the  stomach  and  intestines, 
permitted  by  the  diminution  in  the  atmospheric  pressure 
at  high  altitudes.  Every  year  people  arrive  in  the 
Engadine  with  unsuspected  heart  disease,  which  is  revealed 
or  perhaps  developed  by  palpitation  and  dyspnoea,  render- 
ing a  hasty  retreat  imperative.  On  the  other  hand,  in  a 
case  in  which  the  absence  of  dilatation  and  hypertrophy 
shows  the  valvular  lesion  to  be  slight  and  the  patient  is 
capable  of  all  ordinary  forms  of  exercise  without  suffering, 
high  altitudes  will  usually  give  rise  to  no  inconvenience  or 
danger. 

Moderate  heights,  say  2000  or  3000  feet,  are  usually 
well  borne,  even  when  there  is  decided  valvular  disease, 
and  graduated  exercise  at  such  elevations  is  systematically 
employed  as  a  means  of  improving  the  tone  and  vigour  of 


NECESSITY  OF  COMPLETE  REST.  247 

the  muscular  walls  of  the  heart,  and  of  removing  fatty 
deposit  which  may  have  taken  place  upon  its  surface  and  in 
its  substance. 

Complete  Rest  in  Bed. — Eest  is,  in  many  cases,  an  im- 
portant part  of  the  treatment,  and  when  the  state  of  the 
patient  demands  it,  rest  in  bed  is  of  the  greatest  service  ; 
but  one  of  the  questions  calling  for  the  greatest  exercise 
of  judgment  is  to  decide  when  absolute  rest  is  necessarv. 
There  are  circumstances  in  which  a  month  or  six  weeks  in 
bed  will  prolong  life  for  as  many  years.  On  the  other  hand, 
the  disturbance  of  compensation  and  the  supervention  of 
symptoms  often  date  from  some  slight  injury  which  has 
confined  the  patient  to  his  couch  or  to  the  house  for  a 
month  or  two.  Even  when  severe  symptoms  are  present, 
to  insist  upon  confinement  indoors  is  sometimes  to  add  to 
the  suffering  of  the  last  few  months  of  life  without  adding 
to  its  duration.  When  the  onset  or  exacerbation  of 
symptoms  is  distinctly  attributable  to  work  persisted  in 
from  necessity,  as  in  the  case  of  most  hospital  patients,  or 
from  courage  and  defiance  of  pain,  as  we  sometimes  see ; 
or  when  the  aggravation  is  due  to  imprudent  exertion  or 
exposure,  or  to  some  intercurrent  pulmonary  complication 
or  other  illness,  there  can  be  no  hesitation  in  ordering  rest. 
The  doubt  arises  in  cases  in  which  the  effects  of  valvular 
disease  are  gradually  creeping  on,  and  the  increasing 
breathlessness  and  evening  oedema  are  the  direct  result  of 
the  obstruction  to  the  circulation  and  of  failing  compensa- 
tion. Under  such  circumstances  it  is  difficult  to  decide 
when  to  interfere.  The  patient  will  say  he  is  worse  in  bed 
than  up,  that  he  cannot  lie  down,  but  has  to  be  propped  up 
by  pillows  ;  that  he  cannot  and  dare  not  sleep,  and  that  if 
he  drop  off  into  a  dose  he  wakes  up  in  indescribable  fright 
and  distress.  His  attendants,  it  is  true,  may  tell  us  that  he 
has  had  more  sleep  than  he  supposes,  but  all  the  same  the 
nights  are  long  and  miserable,  and  it  is  no  light  matter  to 


248  HEART  DISEASE. 

condemn  a  sufferer,  who  has  looked  and  longed  for  morning, 
to  a  couch  which,  in  his  experience,  is  associated  with  his 
worst  moments.  Not  uncommonly,  however,  after  sleepless 
tossing  till  early  morning,  with  inability  to  lie  down, 
quiet  sleep  may  come,  and  the  sufferer  may  slip  down 
into  a  comfortable  position  in  which  he  gets  real  repose, 
and  sometimes  after  twenty-four  or  forty-eight  hours  in 
bed,  relief  is  experienced,  which  reconciles  the  patient  to 
the  confinement.  We  must  be  guided  by  results  and  by 
our  knowledge  of  the  patient. 

A  similar  difficulty  frequently  confronts  us  in  advanced 
stages  of  heart  disease,  especially  when  attended  with 
dropsy.  The  patient  implores  us  to  be  allowed  to  sit  up, 
and  in  paroxysms  of  dyspnoea  he  is  compelled  to  do  so  and 
to  throw  his  legs  out  of  bed  and  let  them  hang  down.  It 
is  an  unequivocal  dictate  of  experience,  not  easily  accounted 
for  by  theory,  that  the  heart  in  disease  is  often  relieved  by 
an  upright  posture  of  the  body  and  a  dependent  position  of 
the  legs.  Such  is  the  case,  not  merely  because  in  dropsy 
the  swollen  abdomen  and  thighs  make  it  impossible  to  sit 
well  forward  in  bed  when  the  legs  are  raised,  but  because 
in  some  way  the  position  facilitates  the  action  of  the  heart, 
it  may  be  by  taking  off  the  pressure  of  the  abdominal 
viscera  from  the  diaphragm,  or  by  allowing  blood  to 
gravitate  from  the  right  auricle  into  the  vena  cava  inferior 
and  abdominal  veins,  or  it  may  be  in  consequence  of  a 
physiological  diminution  of  the  arterial  tension  which, 
according  to  Dr.  Oliver,  attends  the  erect  position.  There 
are  few  medical  men  of  large  experience  who  have  not  seen 
instances  in  which  the  sufferer  has  not  gone  to  bed  for 
months,  but  has  slept  all  this  time  in  an  armchair  with 
some  support  contrived  for  the  head.  On  the  other  hand, 
our  results  are  better  when  the  patient  can  be  kept  in  bed ; 
there  is  a  better  chance  of  removal  of  dropsical  effusion  and 
of  recovery  generally  in  the  recumbent  position.     While, 


STIMULANTS.  .  249 

therefore,  we  do  not  carry  too  far  our  resistance  to  a 
patient's  entreaties  to  be  allowed  to  sit  up  in  a  chair  for 
a  part  or  the  whole  of  a  day,  recognizing,  also,  that  a  few 
days  or  weeks  of  life  may  be  dearly  purchased  if  it  is  at  the 
expense  of  increased  suffering,  it  is  our  duty  sometimes, 
and  especially  when  there  is  a  chance  of  recovery  from 
the  existing  complications,  to  exercise  firmness  in  keeping 
the  patient  in  bed  in  spite  of  great  temporary  distress. 

There  is  less  uncertainty  with  regard  to  exposure  to 
cold,  though  in  an  advanced  stage  the  patient  often 
complains  of  subjective  heat,  and  throws  off  his  coverings, 
or  insists  on  the  window  being  opened  on  the  coldest  day 
to  satisfy  his  want  of  air.  External  cold  contracts  the 
arterioles  of  the  surface,  and  increases  the  resistance  in 
the  systemic  circulation,  and  it  should  be  prevented  from 
reaching  the  sufferer.  The  open  window,  however,  may  be 
permitted,  on  condition  that  the  patient  is  efficiently  pro- 
tected. The  play  of  cool,  fresh  air  on  the  face,  and  a  deep 
draught  of  it  into  the  lungs,  are  indescribably  refreshing. 
The  cold  and  livid  lower  limbs  in  aggravated  dropsy  appear 
to  be  almost  insensible  to  changes  of  temperature,  but  they 
should  none  the  less  be  carefully  covered. 

Diet. — Little  need  be  said  about  nourishment.  The 
patient  may  have  whatever  he  can  eat  and  digest,  but  his 
appetite  will  leave  deficiencies,  which  must  be  supplied 
partly  by  liquid  food  of  different  kinds,  and  partly  of  pre- 
parations of  pounded  meat,  fish,  or  chicken. 

When  dropsy  is  present  the  use  of  common  salt  and 
of  chlorides  in  general  should  be  restricted  as  far  as  pos- 
sible, for  the  reasons  given  in  the  chapter  on  dilatation, 
page  308. 

Stimulants. — Alcoholic  stimulants  afford  valuable  help, 
and  will  be  required  more  or  less  in  every  case  of 
severity.  At  first  a  small  quantity  of  any  wine  which  suits 
the  patient  may  be  taken  with  food,  and  frequently  a  little 


250  HEART  DISEASE. 

spirit  in  hot  water  at  night  will  help  to  procure  sleep. 
Ultimately  stimulants,  especially  spirits,  may  have  to  be 
given  freely;  but  great  caution  must  be  exercised  in  the 
early  periods,  since  the  struggle  against  the  encroach- 
ments of  the  malady  is  often  very  long  and  trying,  and  if 
the  good  effects  of  alcohol  are  exhausted  by  abuse  of  it, 
the  patient  is  left  without  resource  when  the  time  of  greatest 
need  arrives.  As  to  the  actual  amount  required,  I  should 
consider  about  six  ounces  of  brandy  per  diem  the  maximum 
likely  to  be  useful  in  the  most  urgent  cases.  This  should 
be  reached  very  gradually  from  two  or  three  ounces,  and 
whenever  an  emergency  has  led  to  an  increase  of  the 
allowance,  it  should  be  reduced  when  the  occasion  has 
passed.  We  must,  above  all,  be  careful  not  to  be  misled  by 
the  patient's  demands.  He  is  conscious  of  relief  from  the 
stimulant,  and  not  unnaturally  asks  for  it  whenever  the 
oppression  or  depression  becomes  severe  ;  but  it  is  easy  to 
pass  the  limits  of  usefulness,  and  to  produce  a  feeling  of 
depression  which  is  only  reaction  from  an  excess  of  alcohol. 

In  larger  quantities  than  six  ounces  the  effects  become 
uncertain,  and  I  have  often  seen  improvement  from  diminu- 
tion of  a  dose  which  seemed  to  be  imperatively  required. 

Drugs. — When  symptoms  have  arisen  requiring  the  em- 
ployment of  medicinal  treatment,  the  first  question  to  be 
considered  is  whether  the  heart  can  be  relieved,  in  any 
degree,  of  work  to  which  it  is  no  longer  equal.  It  is  very 
rarely  that  this  is  not  the  case,  and  not  uncommonly  a 
lessening  of  stress  upon  the  heart  is  sufficient  of  itself  to 
restore  the  circulatory  equilibrium.  A  diminution  in  the 
volume  of  the  blood  by  eliminants  of  various  kinds,  removal 
of  portal  congestion  and  of  distension  of  the  abdominal  veins 
by  purgatives,  which  will  relieve  the  right  side  of  the  heart 
and  lower  the  arterial  tension,  are  among  the  measures  most 
generally  useful  and  most  commonly  required. 

The  fatal  result  is  reached  through  various  secondary 


TREATMENT  BY  DRUGS.  251 

consequences,  the  prevention  or  removal  of  which  postpones 
the  final  issue,  and  not  only  does  this,  but  also  relieves 
suffering.  These  consequences,  therefore,  must  be  studied, 
and  it  will  be  necessary  to  revert  to  the  modes  of  death  from 
valvular  disease  of  the  heart  and  to  consider  the  tendencies 
thereto  which  we  have  to  counteract.  Leaving  out  of  con- 
sideration thrombosis,  whether  systemic  or  pulmonary,  which 
will  best  be  averted  by  the  prevention  of  stagnation  of 
blood  in  the  heart,  heart  disease  tends  to  the  arrest  of  the 
circulation  in  two  different  ways — by  failure  of  propulsion 
through  the  arteries  and  by  damming  back  in  the  veins. 
It  is  not  to  be  understood  that  one  or  other  of  these 
tendencies  is  alone  in  operation  in  any  given  case  ;  the 
rule  is  that  both  are  present,  as  has  been  already  seen. 
While,  however,  in  most  cases  of  valvular  disease  which 
have  proceeded  so  far  as  to  give  rise  to  serious  symptoms, 
the  double  effect  on  the  circulation — the  damming  back  in 
the  veins  and  the  imperfect  propulsion  through  the  arteries 
— is  recognizable,  one  or  other  will  be  a  primary  tendency, 
and  will  predominate,  and  the  treatment  must  be  directed 
to  the  rectification  of  the  tendency  which  is  most  concerned 
in  placing  life  in  danger.  By  far  the  more  common  is 
venous  stasis,  since  it  not  only  follows  directly  from  both 
forms  of  mitral  disease,  but  may  also  be  a  secondary  result 
of  aortic  disease,  and  it  gives  rise  to  a  characteristic  train  of 
phenomena.  Inadequate  arterial  supply  is  of  itself  more 
likely  to  cause  sudden  death  than  to  produce  symptoms. 

With  venous  obstruction  the  liver  will  be  enlarged  and 
greatly  congested,  perhaps  pulsating,  and  one  of  the  first 
objects  of  treatment  is  the  relief  of  this  engorgement  of  the 
liver.  Thereby  relief  will  also  be  afforded  to  the  nausea 
and  sickness  dependent  on  the  congested  state  of  the 
gastro-intestinal  mucous  membrane,  and  also  to  the  over- 
distended  right  side  of  the  heart,  which  is  constantly 
receiving  from  the  liver,  which  acts  as  a  kind  of  reservoir, 


252  HEART  DISEASE. 

more  blood  than  the  right  ventricle  can  transmit  through 
the  lungs.  The  means  to  be  employed  for  the  purpose  are 
chiefly  aperients,  and  all  purgatives  will  have  the  desired 
effect  in  a  greater  or  less  degree ;  but  it  is  not  a  matter  of 
indifference  what  drugs  we  employ.  The  best  results  are 
undoubtedly  to  be  obtained,  according  to  my  experience, 
from  purgatives,  in  which  calomel  or  other  mercurial 
preparation  is  a  constituent,  such  as  calomel  and  compound 
jalap  powder,  calomel,  blue  pill,  or  grey  powder,  with 
colocynth  and  hyoscyamus,  followed  or  not  by  salines. 
Hydragogue  cathartics  of  greater  violence  may  be  necessary 
in  some  cases,  but  the  effect  on  the  liver  and  heart  is  not 
proportional  to  the  degree  of  purgation,  and  the  relief  of 
dropsy  is  not  due  simply  to  the  amount  of  liquid  carried  off 
by  the  intestinal  surface,  but  is  frequently  the  effect  rather 
of  the  diuresis  which  follows  improvement  in  the  circulation. 
Digitalis  is  often  useless,  and  appears  only  to  add  to  the 
embarrassment  of  the  heart- and  to  produce  sickness,  until 
the  way  has  been  cleared  for  its  operation  by  a  mercurial 
purge,  and  where  its  good  effects  on  the  heart  seem  to  be 
expended,  a  fresh  start  will  often  follow  a  calomel  and 
colocynth  pill. 

A  troublesome,  watery  diarrhoea,  which  is  not  unfre- 
quently  present,  is  no  contra-indication  for  purgatives,  but, 
on  the  other  hand,  constitutes  a  distinct  call  for  a  decided 
aperient.  It  is  due  to  the  passive  congestion  of  the  gastro- 
intestinal mucous  membrane  which  results  from  the  obstruc- 
tion in  the  portal  system,  and  is  relieved  by  free  secretion 
from  the  mucous  surface  and  from  the  liver. 

Venesection. — But  the  venous  obstruction  may  reach  a 
point  which  it  is  out  of  the  power  of  purgatives  to  affect. 
The  lower  edge  of  the  liver  is  at  or  near  the  level  of  the 
umbilicus  (or  this  organ  may  be  prevented  from  swelling  by 
cirrhosis),  the  right  cavities  of  the  heart  are  almost  paralyzed 
bv  over-distension,   which,  with  regurgitation  through  the 


VENESECTION.  253 

tricuspid  orifice,  reduces  the  trausmissiou  of  blood  through 
the  lungs  to  a  minimum,  and  the  left  ventricle  receiving 
little  blood  has  little  to  forward  into  the  arterial  system. 
The  pulse  is  weak,  small,  irregular,  both  from  the  irregular 
action  of  the  heart  usually  present,  and  from  some  of  its 
beats  not  reaching  the  wrist.     Unless  the  circulation  is  to 
come  to  a  standstill  the  right  side  of  the  heart  must  be 
promptly  relieved  of  the  over-distension  which  is  the  imme- 
diate cause  of  the  threatened  arrest,  and  this  can  be  most 
quickly  and  effectually  done  by  venesection.      The  with- 
drawal of  a  few  ounces  of  blood  (8-16)  so  far  reduces  the 
pressure  in  the  right  auricle  and  ventricle  when  the  latter 
is  checked  at  the  very  beginning  of  its   systole  by  resist- 
ance which  it  is  unable  to  overcome,  that  it  regains  com- 
mand over  its  contents,  and  is  once  more  able  to  drive  the 
blood  through  the  lungs.     Nothing  can  be  more  striking  or 
satisfactory  than  the  effect  of  bleeding  from  the  arm  under 
such  conditions.     The  face  may  be  livid  and  bedewed  with 
cold  sweat,  the  extremities  blue  and  cold,  but  as  the  blood 
flows  warmth  and  colour  will  return,  the  dyspnoea  will  be 
relieved,  and  the  pulse  will  improve.     The  condition  of  the 
right  ventricle  is  of  critical  importance  when  venesection 
appears  to  be  required.     If  it  is  weak  and  degenerated, 
and  unable  to  take  advantage  of  the  relief  afforded  by  the 
withdrawal  of  blood,  the  desired  result  does  not  follow.    We 
ought,  therefore,  for  bleeding  to  be  successful,  to  have  a 
powerful   right  ventricle   impulse   heaving  the   left  costal 
cartilages,  and  perhaps  the  lower  end  of  the  sternum  itself, 
and  felt  below  the  costal  margin. 

In  some  cases,  where  the  circulation  is  so  nearly  at  a 
standstill  that  blood  will  not  flow  from  the  vein  when 
opened,  a  hypodermic  injection  of  ether  or  strychnia  in  the 
precordial  region  may  cause  the  blood  to  start  flowing,  and 
save  the  patient  from  impending  death. 

Very    frequently,   especially    in  hospital  patients,   the 


254  HEART  DISEASE. 

desired  relief  may  be  obtained  by  leeches,  and  I  have 
usually  selected  the  region  of  the  liver  for  their  applica- 
tion, not  of  course  with  the  idea  of  taking  blood  from  this 
organ,  but  because  there  is,  as  a  rule,  local  pain  here  which 
is  relieved :  six  or  eight  may  be  applied  at  a  time.  The 
abstraction  of  blood  will  be  followed  up  by  a  mercurial 
purge  and  digitalis.  Brandy  and  other  stimulants  may  be 
given  at  the  same  time ;  there  is  nothing  inconsistent  in 
helping  the  oppressed  organ  at  the  same  time  that  it  is 
being  relieved  from  the  special  difficulty  with  which  it  has 
to  contend. 

When,  as  in  aortic  incompetence,  a  spasmodic  and 
imperfect  supply  of  blood  is  the  cause  likely  to  lead  to 
arrest  of  the  circulation,  there  is  no  such  conspicuous  train 
of  symptoms.  There  may  be  precordial  pain,  dyspnoea, 
syncopal  attacks,  etc. ;  but  since  a  momentary  failure  of 
the  circulation  in  the  vital  nerve  centres  is  fatal,  sudden 
death  may  occur  before  the  warnings  of  danger  have 
arrested  attention.  Such  warnings  are  sudden  attacks  of 
faintness  and  dimness  of  vision,  giddiness,  anginoid  pains, 
sudden  weakness  and  trembling  of  the  knees. 

In  this  condition,  measures  suitable  for  the  relief  of 
venous  stagnation  would  be  fatal.  We  cannot  resort  to 
bleeding  ;  purgation  must  be  employed  with  caution.  The 
treatment  must  rather  be  directed  to  stimulation  of  the 
failing  heart,  by  drugs  such  as  strychnine,  ammonia,  and 
ether,  together  with  good,  easily  digested,  nourishing  food, 
and  alcohol  regularly  administered  in  small  quantities. 
Vascular  dilators,  such  as  nitro-glycerine  and  nitrite  of 
amyl  and  sodium  nitrite,  or  perhaps  erythrol,  or  mannitol 
nitrate,  the  effects  of  which  are  more  lasting  according 
to  Bradbury,  may  be  of  great  service  in  cases  in  which 
the  incompetence  is  due  to  degenerative  change  and  not 
to  endocarditis,  especially  where  anginoid  pains  are  a 
prominent  symptom. 


VENESECTION.  255 

Digitalis  may  sometimes  be  of  great  service,  but  its 
effects  are  not  constant,  and  may  be  unfavourable,  or  may 
become  so  after  a  period  of  marked  benefit.  The  reasons 
for  the  apparently  uncertain  and  inconstant  results  of 
digitalis  in  aortic  incompetence  will  be  discussed  in  the 
next  chapter. 


CHAPTER  XVIII. 
TREATMENT  BY  DRUGS. 

use  and  abuse  op  digitalis — substitutes  foe  digitalis 
— the  group  op  cardiac  tonics  of  the  digitalis 
type— their  physiological  action  :  therapeutic 
effects— use  of  digitalis  in  aortic  stenosis,  in 
mitral  incompetence,  in  mitral  stenosis. 

Use  of  Digitalis. 

It  is  too  commonly  taken  for  granted  that  the  existence  of 
valvular  disease  constitutes  an  immediate  indication  for 
the  administration  of  digitalis.  But  to  make  the  discovery 
of  a  murmur  the  signal  for  giving  digitalis  is  fatal  to 
anything  like  precision  in  treatment,  and  may  deprive  the 
sufferer  of  the  advantage  to  be  derived  from  this  remedy 
when  it  is  really  needed.  The  special  indications  for  its 
use  are  frequency,  weakness,  and  irregularity  of  pulse,  and 
oedema  of  the  extremities,  with  scanty,  turbid,  concentrated 
urine.  When  these  are  absent,  it  is  rarely  of  service ;  but 
even  when  these  symptoms  begin  to  show  themselves 
gradually  or  occasionally  on  slight  provocation,  it  will  be 
well  to  combat  them  at  first  with  strychnine,  iron,  quinine, 
and  general  tonics,  rather  than  resort  at  once  to  digitalis, 
the  salts  of  potash  and  any  suitable  vegetable  diuretic 
being  employed  to  promote  secretion  of  urine.  When  the 
use  of  digitalis  is  called  for,  the  most  trustworthy  evidence 
of  its   beneficial   effects  will    be  increase   in  the   amount 


THE   CARDIAC   TONICS.  257 

of  urine  secreted,  with  an  improvement  in  the  tone  and 
vigour  of  the  pulse,  as  well  as  a  more  regular  and  less 
hurried  action  of  the  heart.  When  there  is  no  response 
in  the  form  of  diuresis,  the  pulse  and  general  symptoms 
must  be  carefully  watched  lest  harmful  effects  should 
arise. 

Digitalis  may  be  given  in  combination  with  mix  vomica 
or  strychnia,  or  with  caffein,  or  with  ammonia  or  ether, 
or  various  other  drugs,  according  to  circumstances,  which 
cannot  be  minutely  laid  down.  In  most  cases  it  will  be 
advisable  to  give  a  mercurial  purge  before  its  administration, 
and  to  repeat  this  from  time  to  time. 

In  cases  where  there  is  high  arterial  tension,  the 
exhibition  of  a  mercurial  purgative  from  time  to  time  is 
especially  important,  and  it  may  be  well  to  give  with  the 
digitalis  some  vaso-dilator  such  as  spiritus  setheris  nitrosi, 
liq.  trinitrin,  erythrol  tetranitrate,  etc.,  to  counteract  the 
tonic  effects  of  the  digitalis  on  the  arterioles  and  capil- 
laries. As  alternatives  to  digitalis,  strophanthus,  conval- 
laria,  caffein,  spartein,  cactein  have  been  advocated. 

Convallaria  has  been  extensively  tried,  but  either  its 
effect  or  its  preparation  is  uncertain,  and  it  does  not 
appear  to  be  of  great  service. 

Strophanthus  may  be  a  most  useful  alternative  when 
digitalis  produces  sickness,  and  may  even  succeed  where 
digitalis  has  failed.  It  is  claimed  for  strophanthus  that  its 
tonic  action  is  mainly  confined  to  the  heart,  and  that  it 
does  not  cause  contraction  of  the  arterioles  and  thus  in- 
crease the  peripheral  resistance  in  the  same  way  as  digitalis. 

Caffein  is  said  to  increase  the  solids  in  the  urine, 
which  would  make  it  a  useful  complement  to  digitalis, 
which  promotes  a  flow  of  water.  It  is  also  a  cardiac 
stimulant.  In  my  hands  it  has  often  been  a  most  useful 
accessory  to  digitalis,  diuresis  and  general  improvement 
setting  in  promptly  on  the  administration  of  5  gr.  doses  of 


258  HEART  DISEASE. 

citrate  of  caffein  three  times  a  day  in  addition  to  digitalis, 
which  had  failed  to  produce  any  decided  effect  without 
it.  I  have  not,  however,  found  that  caffein  alone  is  an 
efficient  substitute  for  digitalis. 

Theobromine  and  diuretin,  the  latter  of  which  is  a  sodio- 
salicylic  compound  of  theobromine,  are  powerful  diuretics, 
and  have  a  similar  stimulant  action  on  the  heart  to  caffein ; 
they  may  be  used  with  advantage  in  cases  of  cardiac 
dropsy,  and  sometimes  succeed  where  caffein  fails. 

Digitalis  and  its  congeners,  which  contribute  the  most 
important  group  of  cardiac  tonics,  possess  special  interest, 
and  merit  a  separate  discussion,  since  they  not  only 
render  important  service  in  the  treatment  of  disease,  but 
furnish  one  of  the  best  illustrations  of  the  relation  between 
physiological  and  therapeutic  action.  Digitalis,  the  best 
known  and  longest  employed,  as  well  as  the  most  important 
of  them,  will  be  taken  as  the  general  representative  of 
the  class.  Their  physiological  action  will  first  be  briefly 
mentioned. 

Their  Physiological  Action. 

The  physiological  action  is  a  stimulation  of  the  muscular 
fibres  of  the  entire  cardio-vascular  system,  giving  rise,  on 
the  one  hand,  to  more  deliberate  and  powerful  action  of  the 
heart,  and  on  the  other  to  tonic  contraction  of  the  arterioles 
and  capillaries.  After  death  from  the  poisonous  effect  of 
digitalis,  the  arterioles  are  narrowed  to  an  impervious 
thread,  and  the  ventricles  of  the  heart  are  found  firmly 
contracted  upon  themselves,  and  empty.  The  drug  apj)ears 
to  act  directly  upon  the  muscular  structures,  and  not 
through  an  intermediate  influence  upon  nerves ;  we  have 
not,  therefore,  in  considering  the  effects  upon  the  heart,  to 
discuss  the  question  whether  they  are  produced  by  in- 
hibition of  the  sympathetic  or  stimulation  of  the  vagus. 


action  of  digitalis.  259 

Their  Therapeutic  Action. 

There  are  various  ways  in  which  the  physiological 
action  thus  briefly  sketched  may  come  to  the  aid  of  the 
circulation  when  the  transit  of  blood  through  the  heart  is 
hampered  by  valvular  or  other  disease.  Besides  the  more 
complete  expulsion  of  their  contents  by  the  energetic  con- 
traction of  the  ventricles,  which  will  help  to  fill  the 
arterial  side  of  the  circulatory  system,  there  will  be  im- 
proved suction  action  during  diastole,  which  will  tend  to 
withdraw  from  the  veins  the  blood  which  has  been  dammed 
back  and  remains  stagnating  in  the  liver  and  abdominal 
venous  plexuses.  Another  effect  is  that  not  only  are  the 
force  and  effectiveness  of  the  systole  increased,  but  the 
general  vigour  of  the  heart  is  renewed,  through  the  in- 
creased physiological  rest  resulting  from  the  relative  pro- 
longation of  the  diastolic  period,  which  gives  opportunity 
for  nutritive  repair  of  the  cardiac  muscular  fibres,  and  for 
the  reaccumulation  of  energy  expended  in  the  systole. 

The  primary  effect  of  the  tonic  contraction  of  the 
arterioles  will  be  to  increase  the  resistance  in  the  peripheral 
circulation,  thus  throwing  more  work  upon  the  heart ;  and 
it  is  conceivable  that  the  arterio-capillary  contraction  may, 
under  certain  conditions,  more  than  neutralize  the  increased 
force  of  the  ventricular  systole,  as,  for  example,  when  the 
cardiac  muscular  fibres  have  undergone  serious  degenera- 
tion, and,  as  a  matter  of  observation,  this  is  found  some- 
times to  be  the  case.  For  the  most  part,  however,  the 
disease,  and  especially  valvular  disease,  which  has  given 
rise  to  the  necessity  for  cardiac  tonics,  will  have  brought 
about  considerable  hypertrophy  of  the  muscular  walls  of 
the  heart  without  any  corresponding  hypertrophy  of  the 
muscular  walls  of  the  vessels.  The  balance  of  advantage, 
therefore,  when  the  contractile  energy  of  both  heart  and 
vessels  is  increased,  is   largely  on  the  side  of  the   heart, 


260  HEART  DISEASE. 

its  muscular  fibres  having  greatly  increased  in  number 
and  size. 

It  might  seem,  again,  that  the  contraction  of  the 
arterioles  would  more  or  less  intercept  the  vis  a  tergo  in 
the  veins  which  is  already  lacking,  as  is  often  manifested 
by  the  presence  of  cedema.  If,  however,  we  bear  in  mind 
that  the  contraction  affects  not  only  the  arterioles  but  the 
capillaries  also,  it  will  be  evident  that  the  narrowing  of 
these  channels  will  give  rise  to  increased  rapidity  of  the 
current  of  blood  within  them  which  will  carry  to  the 
venules  the  propulsive  force  communicated  by  the  heart 
better  than  a  sluggish  and  irregular  movement  through  a 
network  of  flaccid,  dilated  and  bulging  capillaries.  This 
more  rapid  onward  flow  of  the  blood  will  again  favour  the 
taking  up  of  fluid  effused  into  the  inter-cellular  spaces. 

It  would  seem  that  the  effects  just  enumerated  ought  to 
be  of  equal  service  in  all  forms  of  heart  disease,  excepting 
structural  degeneration  of  the  walls,  and  certainly  in  all 
forms  of  valvular  disease.  As  a  matter  of  observation,  how- 
ever, such  is  not  found  to  be  the  case.  In  one  valvular 
disease,  mitral  incompetence,  all  observers  agree  that 
digitalis  is  of  the  greatest  possible  service  ;  in  another, 
mitral  stenosis,  there  is  almost  equal  concurrence  of  opinion 
that  this  remedy  is  not  of  the  same  benefit,  and,  indeed, 
that  it  is  capable  of  doing  harm  and  of  aggravating  the 
bad  effects  of  the  disease.  In  aortic  incompetence  orjinions 
are  divided,  some  maintaining  that  the  cardiac  tonics  in 
general  and  digitalis  in  particular  are  injurious,  others 
that  they  are  helpful.  The  same  may  be  said  of  aortic 
stenosis. 

It  appears  to  me  that  an  explanation  of  this  difference, 
if  it  can  be  arrived  at,  will  make  our  comprehension  of  the 
beneficial  effect  more  clear,  and  render  our  employment  of 
these  remedies  more  precise. 

The  question  of  the  effects  of  digitalis  is  often  argued 


DIGITALIS  IN  AORTIC  DISEASE.  261 

on  theoretical  grounds ;  but  it  must  be  pointed  out  that  it 
is  upon  experience  and  not  upon  theoretical  considerations 
that  the  conclusion  just  stated  as  to  the  difference  in  its 
remedial  influence  is  based.  Long  before  the  physiological 
action  of  digitalis  was  ascertained,  it  had  been  noted  that 
this  remedy  was  not  always  beneficial  in  its  action,  and  was 
sometimes  obviously  injurious,  and  much  was  said  by  old 
writers  as  to  intolerance  of  the  drug  and  especially  as  to  its 
cumulative  effects.  When  mitral  stenosis  was  not  distin- 
guished from  incompetence  of  this  valve,  the  varying 
effects  of  digitalis  must  have  been  most  perplexing,  and, 
indeed,  incomprehensible. 

In  aortic  regurgitation  failure  of  compensation  is 
manifested  in  two  distinct  ways,  and  there  are  two  different 
modes  of  death.  In  one,  the  effect  is  defective  propulsion 
of  blood  into  the  arterial  system,  manifested  by  faintness, 
giddiness,  and  sudden  weakness  of  the  legs,  sometimes  by 
anginoid  pain ;  death  is  by  syncope ;  in  the  other,  there  is 
obstructive  backworking  through  the  lungs  and  right  heart, 
giving  rise  to  venous  obstruction  and  dropsy,  exactly  as  in 
mitral  insufficiency.  There  are,  in  effect,  aortic  physical 
signs  with  mitral  symptoms. 

We  have  in  this,  it  appears  to  me,  an  explanation  of  the 
different  views  as  to  the  influence  of  digitalis  in  aortic  in- 
sufficiency. When  the  tendency  indicated  by  the  symptoms 
is  defective  propulsion  with  failure  of  arterial  blood  supply 
to  the  brain,  the  effects  are  uncertain  and  even  doubtful. 
While  sometimes  apparently  beneficial  for  a  while,  a 
frequent  result  is  the  production  of  irregularity  of  the  pulse 
with  aggravation  of  the  symptoms,  and  occasionally  of 
vomiting  attended  with  rapidly  increasing  weakness  of  the 
heart's  action.  Cases  are  met  with,  indeed,  in  which  there 
is  grave  reason  to  suspect  that  it  has  precipitated  a  sudden 
fatal  termination. 

When,  on  the  other  hand,  the  symptoms  are  due  to 


262  HEART  DISEASE. 

secondary  dilatation  of  the  left  ventricle  not  adequately- 
neutralized  by  hypertrophy,  with  or  without  mitral  regurgi- 
tation, and  to  the  effects  of  this  upon  the  pulmonary 
circulation  and  right  ventricle,  we  have  exactly  the  same 
opportunity  for  the  beneficial  influence  of  digitalis  in 
reinforcing  the  right  side  of  the  heart,  and  the  same 
favourable  results  as  in  mitral  regurgitation.  The  effects, 
indeed,  are  sometimes  much  more  striking,  and  the  removal 
of  dropsical  effusion  more  rapid.  I  have  observed,  however, 
that  not  uncommonly  patients  suffering  from  serious  aortic 
insufficiency,  after  recovering  from  the  mitral  symptoms,  die 
suddenly  from  failure  of  the  left  ventricle,  and  this  whether 
the  digitalis  has  been  continued  or  left  off,  and  sometimes 
before  the  patient  has  begun  to  get  up  and  move  about. 

Aortic  stenosis,  like  aortic  incompetence,  leads  up  to  a 
fatal  termination  in  two  ways — directly,  by  limiting  the 
supply  of  arterial  blood,  and  indirectly,  by  giving  rise  to 
back  pressure  in  the  pulmonic  and  venous  circulation, 
through  secondary  mitral  incompetence.  It  is  only  when 
symptoms  arise  from  the  latter  that  digitalis  is  useful. 
In  the  earlier  stages  the  left  ventricle  may  be  injured  if 
stimulated  to  drive  its  contents  through  a  narrowed  orifice. 
More  relief  is  often  obtained  by  relaxing  the  arterioles 
by  means  of  nitroglycerine,  deducting  thus  the  arterio- 
capillary  resistance  from  the  total  work  with  which  the 
heart  has  to  contend. 

Mode  of  Action  of  Digitalis  in  Mitkal 
Eegukgitation. 

Mitral  regurgitation,  being  the  disease  in  which  the 
action  of  the  cardiac  tonics  is  almost  always  beneficial,  a 
study  of  the  conditions  presented  may  enable  us  to  arrive 
at  some  comprehension  of  the  way  in  which  the  good  effects 
are  brought  about. 


DIGITALIS  IN  MITRAL   INCOMPETENCE.  363 

What  takes  place  in  mitral  regurgitation  is  as  follows : 
The  regurgitation  into  the  left  auricle  dilates  this  cavity 
(there  may  be  some  hypertrophy  of  its  muscular  walls,  but 
no  compensatory  influence  of  any  consequence  is  gained 
thereby)  and  at  the  same  time  drives  back  the  blood  which 
is  flowing  to  the  left  auricle  and  ventricle  by  the  pulmonary 
veins.  The  obstruction  in  the  pulmonary  veins  necessarily 
gives  rise  to  resistance  to  the  onward  flow  through  the 
capillaries,  to  overcome  which  increased  pressure  is  required 
in  the  pulmonary  artery,  and  therefore  greater  driving 
power  on  the  part  of  the  right  ventricle.  From  this  results 
hypertrophy  of  the  right  ventricle,  which  is  the  great 
compensating  agency  by  which  the  leakage  of  the  mitral 
valve  is  more  or  less  perfectly  neutralized.  If  the  blood 
pressure  in  the  pulmonary  veins  could  be  maintained  at 
such  a  point  as  to  be  greater  than  the  pressure  in  the  aorta, 
there  would  be  no  reflux  into  the  auricle  durina;  the  con- 
traction  of  the  ventricle,  even  were  the  mitral  valve 
completely  destroyed;  but,  however  powerful  the  action  of 
the  right  ventricle,  this  can  never  be  absolutely  the  case. 
The  walls  of  the  pulmonary  capillaries  and  veins  and  of 
the  left  auricle,  are  too  weak  to  resist  such  a  distending 
force,  and  moreover  the  suction  action  of  the  left  ventricle 
during  diastole  will  always  temporarily  reduce  the  pressure 
in  the  left  auricle. 

Another  change  in  the  heart  resulting  from  mitral 
regurgitation  must  be  noticed.  This  is,  a  dilatation  of  the 
left  ventricle,  produced  by  distension  of  this  cavity  during 
the  defenceless  diastolic  period,  by  the  high  pressure  in  the 
pulmonary  veins  and  left  auricle.  It  involves  some  con- 
secutive hypertrophy  of  the  ventricular  walls. 

These  familiar  and  elementary  explanations  are  enume- 
rated in  order  once  more  to  emphasize  the  fact  that  the 
work  of  compensation  for  mitral  regurgitation  falls  upon 
the     right    ventricle,    and     that,   when     systemic    venous 


264  HEART  DISEASE. 

stasis  and  other  late  effects  of  mitral  regurgitation  show 
themselves,  it  is  because  the  right  ventricle  is  beaten 
by  the  resistance  in  the  pulmonary  circuit  and  can  no 
longer  keep  up  adequate  pressure  in  the  left  auricle. 

Applying  now  our  knowledge  of  the  physiological 
effects  of  digitalis,  we  shall  see  that  the  favourable  results 
of  its  administration  are  due  almost  entirely  to  reinforce- 
ment of  the  right  ventricle.  On  the  left  side  of  the  heart 
and  in  the  systemic  circulation  there  will  be  produced  a 
certain  degree  of  arterio-cajjillary  contraction,  with  slight 
increase  in  the  peripheral  resistance  and  in  the  intermediate 
arterial  tension,  and  a  more  deliberate  and  energetic  action 
of  the  left  ventricle  in  systole,  which  makes  room  for  a 
large  volume  of  blood  in  diastole,  while  the  elastic  rebound 
at  the  end  of  systole  exercises  a  better  suction  action  on  the 
contents  of  the  distended  left  auricle.  The  hypertrophy 
of  the  ventricular  walls,  which  will  more  than  neutralize 
the  increase  of  resistance  in  the  peripheral  circulation,  and 
the  greater  capacity  of  the  cavity  would,  in  the  absence  of 
regurgitation  into  the  auricle,  result  in  the  projection  of 
a  larger  charge  into  the  arteries  at  each  systole.  The  effect 
of  this  is  undoubtedly  good,  but  the  regurgitation  into  the 
left  auricle  is  a  set-off  against  it,  and  this  will  be  increased 
with  the  increase  of  resistance  in  the  arterial  system.  So 
far,  however,  as  these  good  effects  on  the  left  ventricle  and 
systemic  circulation  are  concerned,  they  would  be  much 
more  conspicuous  in  aortic  regurgitation  than  in  mitral 
regurgitation,  since  the  ventricle  is  stronger  and  its 
capacity  larger,  and  yet  we  do  not  find  that  digitalis  is 
more  useful  in  this  affection,  but  very  often  the  contrary. 

Looking  now  at  the  effects  upon  the  right  side  of  the 
heart  and  the  pulmonary  circuit,  there  may  or  may  not  be 
contraction  of  the  arterioles  and  capillaries  in  the  lungs 
with  increase  of  resistance.  This  could,  however,  in  any 
case    only   be   slight,    while   the   ventricular    walls    being 


DIGITALIS  IN  MITRAL   INCOMPETENCE.  265 

greatly  hypertrophied,  increase  of  vigour  in  their  con- 
traction will  at  once  raise  the  blood  pressure  in  the  entire 
pulmonary  circulation  and  in  the  left  auricle.  Improved 
pressure  in  the  left  auricle,  as  has  been  seen,  will  fill 
the  left  ventricle  better  during  diastole,  will  resist  reflux 
through  the  mitral  orifice  in  the  systole,  and  so  will 
increase  the  amount  of  blood  thrown  into  the  aorta. 

It  is  here  that  the  beneficial  influence  of  digitalis  really 
comes  in.  As  has  been  before  stated,  the  neutralization  of 
the  effects  of  mitral  regurgitation  is  almost  entirely  the 
work  of  the  right  ventricle,  and  it  is  by  increasing  the 
efficiency  of  its  compensatory  action  that  digitalis  is  of 
service.  Additional  evidence  of  this  is,  on  the  one  hand, 
the  fact  that  relief  of  over-distension  of  the  right  side  of 
the  heart  by  venesection  or  leeches  and  purgation  is  an 
important  corroborative  measure,  in  many  cases  absolutely 
essential  to  the  result,  and,  on  the  other  hand,  that  digitalis 
fails  when  the  right  ventricle  is  seriously  degenerated  or 
hampered  by  pericardial  adhesions. 

Among  the  conspicuous  favourable  results  of  the  ad- 
ministration of  digitalis  is  diminished  irregularity  of  the 
pulse.  This  is  entirely  due  to  the  higher  blood  pressure 
in  the  left  auricle,  and  the  more  regular  supply  of  blood  to 
the  ventricle.  Mitral  incompetence  is  the  one  among  the 
valvular  affections  which  is  specially  liable  to  give  rise  to 
irregularity  of  the  pulse.  This  will  be  understood  from 
the  following  considerations.  The  left  auricle  is  exposed  to 
the  respiratory  variations  of  pressure  which  its  thin  walls 
resist  only  imperfectly.  When,  therefore,  these  variations 
are  exaggerated,  as  when  the  breath  is  held  or  when  there 
is  dyspnoea  from  bronchitis  or  asthma,  the  amount  of  blood 
carried  on  into  the  left  ventricle  will  vary,  and  the  pulse 
will  be  more  or  less  irregular.  During  inspiration  the 
negative  pressure  will  tend  to  keep  the  auricle  dilated,  and 
to  prevent  it  from  contracting  properly,  so  that  the  ventricle 


266  HEART  DISEASE. 

will  not  have  a  full  charge  of  blood,  and  its  systole  will  be 
brief  and  abortive.  During  forced  expiration  the  auricle  will 
be  compressed,  and  its  contained  blood  will  be  forced  on 
into  the  ventricle,  with  opposite  consequences.  In  mitral 
regurgitation  a  further  effect  will  be  that  the  negative  pres- 
sure of  inspiration  will  encourage  the  reflux  into  the  auricle, 
while  the  positive  pressure  of  expiration  will  oppose  it. 
In  this  way — the  ventricle  sometimes  being  imperfectly,  at 
other  times  perfectly,  filled,  sometimes  sending  back  more, 
sometimes  less,  of  its  contents  into  the  auricle — we  have 
ample  explanation  of  irregularity  of  the  pulse.  Now,  the 
lower  the  internal  blood-pressure  in  the  auricle  and  pul- 
monary veins,  the  greater  will  be  the  effect  of  variations  of 
external  pressure,  and  the  higher  the  pressure  within  the 
auricle,  the  more  independent  it  will  be  of  pressure  from 
without.  It  will  be  seen,  therefore,  how  digitalis  steadies 
the  action  of  the  heart  and  renders  the  pulse  more  regular. 

Effects  of  Digitalis  in  Mjtkal  Stenosis. 

If  we  examine  the  effects  of  digitalis  in  mitral  stenosis, 
we  may  perhaps  see  why  they  are  less  certainly  favourable, 
and  sometimes  clearly  unfavourable.  In  an  uncomplicated 
case  the  left  ventricle  is  neither  dilated  nor  hypertrophied, 
and  the  arteries  generally  are  already  small  and  contracted. 
No  obvious  advantage  can  be  seen  in  further  contraction 
of  the  arterioles,  and,  in  point  of  fact,  the  symptoms  are 
somewhat  relieved  by  causing  them  to  dilate.  No  great 
improvement  in  the  output  of  blood,  again,  is  to  be  gained 
by  more  vigorous  contraction  of  the  walls  of  the  left 
ventricle,  as  they  are  not  specially  strong,  and  the  cavity  is 
small.  But  it  would  seem  that  increased  vigour  in  the 
contraction  of  the  right  ventricle  should  have  the  same 
good  effect  here  as  in  mitral  regurgitation,  and  marked 
beneficial  influence  is  indeed  very  commonly  observed  if 
it  is  judiciously  administered  when  the  right  ventricle  is 


DIGITALIS  IN  MITRAL  STENOSIS.  267 

beginning  to  give  way.  The  conditions,  however,  are 
different,  and  if  given  in  the  early  stages  of  mitral  stenosis 
it  may  do  actual  harm.  In  mitral  regurgitation  the 
increased  amount  of  blood  driven  by  the  right  ventricle 
into  the  pulmonary  artery,  by  raising  the  pressure  in  the 
pulmonary  circulation,  antagonizes  the  reflux  into  the 
auricle,  so  that  more  blood  finds  its  way  into  the  left 
ventricle,  whereas  in  mitral  stenosis  the  blood  cannot  be 
forced  through  the  constricted  mitral  orifice  beyond  a 
certain  rate  of  speed,  and  if  the  right  ventricle  is  stimu- 
lated to  contract  more  than  is  required  for  this,  it 
encounters  an  insuperable  obstruction,  and  becomes  em- 
barrassed in  its  action,  its  energy  being  uselessly  expended. 
A  common  result  is  irregularity  in  the  beats,  accompanied 
by  a  sense  of  precordial  oppression,  and  not  infrequently 
the  heart-beats  are  in  couples,  the  first  of  which  alone 
reaches  the  wrist,  the  second  having  no  aortic  second 
sound. 

In  many  cases  of  advanced  mitral  stenosis,  in  which 
there  is  fair  compensation,  the  coupled  beats  can  be  pro- 
duced at  will  by  giving  digitalis.  The  second  of  the  two 
beats  is  evidently  a  supplementary  systole  of  the  right 
ventricle :  there  is  a  right  ventricle  impulse  felt  over  the 
lower  left  costal  cartilages,  while  the  apex  beat  is  scarcely, 
or  not  at  all,  perceptible.  At  the  second  of  the  coupled 
beats  both  right  ventricle  sounds  are  heard,  while  the  aortic 
second  sound  is  absent,  and  if  there  is  a  systolic  mitral 
murmur  as  well  as  the  presystolic,  it  is  audible  only  with 
the  first  of  the  two  beats.  When  compensation  has  broken 
down  and  there  are  pulsation  of  the  veins  in  the  neck, 
oedema  of  the  extremities,  and  other  evidence  of  secondary 
tricuspid  regurgitation,  digitalis  may  be  given,  oftentimes 
with  marked  benefit,  but  its  effects  should  be  carefully 
watched,  and  it  should  not  be  persevered  with  too  long  if 
good  results  do  not  follow. 


CHAPTER  XIX. 
STRUCTURAL   CHANGE   IN  THE   HEART. 

HYPERTROPHY — CAUSES  OP  HYPERTROPHY  OP  THE  LEFT 
VENTRICLE,  OF  THE  RIGHT  VENTRICLE — PHYSICAL  SIGNS 
— SYMPTOMS— PROGNOSIS— TREATMENT. 

The  muscular  walls  of  the  heart  are  liable  to  changes  of 
various  kinds,  some  of  which  constitute  diseases  which 
shorten  life  and  give  rise  to  much  suffering.  Of  these 
structural  alterations,  some  are  common — hypertrophy, 
dilatation,  fatty  degeneration,  fibrosis ;  others  rare — cancer, 
syphilitic  gumma,  abscess,  aneurysm.  We  shall  concern 
ourselves  mainly  with  those  which  are  comparatively 
frequent;  the  others,  obscure  as  well  as  uncommon,  are 
very  seldom  recognized  during  life,  and  a  diagnosis  is  only 
made  when  an  exceptionally  clear  case  comes  under  the 
notice  of  an  exceptionally  acute  observer. 

Even  when  the  common  and  familiar  affections — hyper- 
trophy, dilatation,  and  degeneration — only  are  taken  into 
consideration,  we  find  ourselves  on  much  less  secure  ground 
than  when  dealing  with  lesions  of  the  valves.  The  latter 
we  can  localize  with  great  confidence ;  and  knowing,  partly 
by  experience,  partly  by  the  application  of  mechanical 
principles,  their  effects  and  tendencies,  we  can,  by  making 
out  how  far  such  effects  are  manifest,  form  an  opinion  as  to 
the  probable  course  of  the  symptoms  and  as  to  the  future  of 
the  patient.  On  examination  after  death,  again,  we  can 
understand    the    connection    between    the    lesion    and    the 


STRUCTURAL    CHANGE  IN  THE  HEART   WALLS.       26c, 

symptoms,  and  can  follow  the  sequence  of  secondary 
changes  in  the  heart  and  vessels  which  are  set  up  by  the 
original  valvular  defect.  In  the  case  of  structural  changes, 
on  the  contrary,  the  diagnosis  cannot  be  made  with  the 
same  precision,  and  we  are  often  left  in  some  degree  in  the 
dark  even  by  a  post-mortem  examination.  In  one  patient 
fatty  degeneration  has  apparently  proved  fatal  at  so  early 
a  stage  that  the  naked-eye  characters  of  the  condition  are 
scarcely  perceptible,  and  it  is  only  by  the  microscope  that 
its  existence  is  definitely  established ;  in  another  the 
change  has  proceeded  so  far  that  the  fingers  sink  into  the 
pale  greasy  walls,  and  the  muscular  fibres  have  almost 
disappeared,  so  that  it  is  scarcely  conceivable  how  the 
heart  has  been  able  to  impress  any  movement  whatever 
011  the  blood,  or  how  life  has  been  sustained  through  the 
intermediate  stages  of  disintegration.  So  with  regard  to 
dilatation,  there  is  no  fixed  relation  between  the  degree  of 
enlargement  of  the  cavities  and  thinning  of  the  walls  found 
after  death  and  the  interference  with  the  circulation 
observed  during  life.  One  man  will  live  for  years  with 
a  heart  which  has  reached  the  extreme  limits  of  dilatation, 
while  another  succumbs  when  it  is  but  moderately  advanced. 
If,  therefore,  we  could  make  out  with  great  exactness  the 
dimensions  of  the  heart,  the  size  of  its  separate  chambers, 
and  the  thickness  of  their  respective  walls,  which  is  no  easy 
task,  we  could  not  on  these  grounds  alone  compare  one  case 
with  another,  and  decide  upon  the  relative  danger. 

Many  other  considerations  of  extreme  importance  will 
come  into  the  estimate — the  functional  vigour  of  the 
muscular  walls  as  well  as  their  thickness,  the  liability  to 
palpitation,  the  state  of  the  great  and  small  vessels,  the 
degree  of  peripheral  resistance,  the  presence  or  absence  of 
reflex  irritation  of  the  heart  from  gastric  or  other  derange- 
ment. The  question  of  prognosis  thus  becomes  extremely 
complicated,  and  is  beset  with  uncertainty.     An  element  of 


270  HEART  DISEASE. 

chance  or  luck  even  comes  in — the  subject  of  advanced 
disease  is  at  the  mercy  of  the  slightest  accident;  many  a 
patient  lives  for  years  with  a  dilated  or  fatty  heart  who 
would  be  killed  by  an  attack  of  influenza,  or  by  a  powerful 
emotion,  or  by  tripping  over  a  stone  or  a  mat.  A  serious 
obstacle  to  the  attainment  of  the  minute  and  definite 
knowledge  which  alone  is  of  real  use  in  arriving  at  a  sure 
prognosis  in  structural  disease  of  the  heart,  is  the  fact 
that  a  large  proportion  of  the  cases  occur  in  private  and 
consulting  practice,  and  comparatively  few  come  under 
observation  in  hospital.  It  is  difficult,  therefore,  to  keep 
such  cases  in  sight  and  to  watch  their  progress,  and  seldom 
possible  to  obtain  a  post-mortem  examination  to  confirm 
the  diagnosis. 

While,  however,  the  great  difficulty  of  prognosis  and 
diagnosis  in  structural  diseases  of  the  heart  is  acknowledged, 
it  is  of  the  utmost  consequence  that  such  approximation  to 
a  forecast  of  the  prospects  of  life  as  is  possible  should  be  an 
object  of  serious  endeavour.  The  cases  are  numerous,  far 
more  numerous  at  and  after  middle  age  than  those  of 
valvular  disease,  and  everything  which  has  been  said  as  to 
the  importance  of  prognosis  in  general  applies  here.  An 
early  recognition  of  these  changes,  indeed,  is  often  of 
greater  service  to  the  subject  of  them  than  in  the  case 
of  valvular  affections,  since  it  reveals  also  the  tendencies 
which  are  in  operation,  and  often  at  a  time  when  they  can 
be  successfully  combated  by  treatment. 

Too  commonly,  however,  no  attempt  is  made  to  recog- 
nize the  existence  and  extent  of  degeneration  or  dilatation. 
The  symptoms  due  to  derangement  of  the  circulation  force 
themselves  upon  the  attention  of  the  medical  man,  but  no 
murmur  being  detected,  the  only  diagnosis  ventured  upon 
is  that  of  "weak  heart,"  a  vague  term  which  covers  the 
entire  ground,  from  temporary  functional  debility  to  disease 
inevitably  and  imminently  fatal.     Such  a  diagnosis  reacts 


STRUCTURAL    CHANGE  IN  THE   HEART   WALLS.       271 

unfavourably  upon  the  mind  of  the  observer  who  rests  upon 
it,  and  makes  him  less  exact  and  trustworthy,  while  it  may 
be  full  of  danger  to  the  patient. 

These  considerations  alone  would  justify  an  attempt  to 
render  the  prognosis  of  structural  diseases  of  the  heart 
more  definite,  but  a  study  of  these  affections  from  the 
point  of  view  of  prognosis  also  leads  to  closer  observation, 
and  to  the  recognition  of  the  importance  of  details  which 
do  not  force  themselves  upon  the  attention  so  long  as 
diagnosis  in  the  ordinary  and  limited  sense  of  the  word 
only  is  the  object. 

A  further  justification  of  the  prominence  given  to  prog- 
nosis is  that  the  grasp  of  all  the  facts  of  the  disease  and 
of  the  individual  case,  which  is  necessary  to  the  formation 
of  a  just  forecast  of  the  result,  is  the  best  guide  for 
treatment,  whether  this  may  demand  chiefly  patience  and 
caution,  or  must  be  energetic  and  prompt.  Prognosis  is 
not  merely  a  well-instructed  conjecture  as  to  the  ultimate 
issue,  it  is  a  deliberate  judgment  as  to  the  processes  and 
tendencies  of  the  disease,  and  as  to  the  constitutional 
soundness  and  strength  of  the  patient.  The  foresight 
relates  to  the  dangers  which  attend  the  attack,  to  the 
course  it  will  run,  and  to  the  influences  and  contingencies 
which  make  for  or  against  the  sufferer.  To  this  there  has 
only  to  be  added  a  knowledge  of  the  therapeutic  measures 
by  which  the  tendency  to  death  or  structural  injury  can 
be  antagonized,  and  by  which  the  patient  can  be  guided 
and  helped,  together  with  skill,  courage,  and  promptitude 
in  applying  it,  and  we  have  all  the  requisites  for  successful 
treatment. 

Treatment,  therefore,  will  form  a  natural  sequel  and 
corollary  to  prognosis. 


272  HEART  DISEASE. 


HYPEETEOPHY. 


This  condition  of  the  heart  will  not  detain  us  long.  The 
prognosis  of  cardiac  hypertrophy,  like  the  symptoms,  is  that 
of  its  cause,  and  the  character  and  degree  of  hypertrophy 
are  important,  not  so  much  in  themselves  or  on  account  of 
danger  likely  to  arise  out  of  them,  but  as  indicating  the 
existence  of  some  condition  which  has  given  rise  to  the 
increase  in  thickness  and  contractile  power  of  the  muscular 
walls  of  the  heart,  and  which  is  serious,  possibly,  in  pro- 
portion to  the  hypertrophy  which  it  has  provoked. 

Causes  of  Hypeeteophy  of  the  Left  Venteicle. 

The  causes  which  give  rise  to  hypertrophy  must  be 
enumerated.  The  left  or  right  ventricle  may  be  affected 
alone  or  predominantly,  or  both  may  have  undergone 
change.  The  causes  which  bring  about  hypertrophy  of 
the  left  ventricle  are,  in  the  first  place,  valvular  diseases, 
stenosis,  or  insufficiency  of  the  aortic  valve,  or  mitral 
insufficiency.  With  these  we  are  not  now  concerned, 
as  they  have  been  fully  discussed  in  the  chapters  on  the 
respective  valvular  lesions.  Next  in  frequency  will  be 
protracted  high  arterial  tension.  When  high  pressure  in 
the  systemic  arteries  is  recognized,  and  especially  when 
there  are  evidences  of  its  having  been  habitual  for  some 
time,  such  as  large,  thickened,  tortuous,  radial  and  temporal 
arteries,  or  a  dilated  ascending  aorta,  the  underlying  con- 
dition to  which  it  is  due  must  be  identified.  The  causes  of 
high  arterial  tension  and  the  mechanism  of  its  production 
have  been  dealt  with  in  Chapter  II.,  so  they  will  only  be 
briefly  enumerated  here.  They  are  renal  disease,  gout, 
diabetes,  lead  poisoning,  excessive  nitrogenous  diet,  consti- 
pation, alcohol,  tobacco,  and,  above  all,  a  hereditary  predis- 
position. 

Left  ventricle  hypertrophy,  again,  may  in  rare  instances 


HYPERTROPHY.  273 

have  no  other  assignable  origin  than  adherent  pericardium, 
a  condition  which  is  difficult  to  diagnose,  and  with  regard 
to  which  prognosis  is,  as  a  rule,  unfavourable  if  the  heart  is 
much  enlarged. 

If  hypertrophy  is  at  any  time  produced  by  a  mode  of 
life  entailing  sustained  muscular  exertion,  it  is  physio- 
logical and  not  pathological,  and  has  no  claims  on  our 
attention ;  unless,  indeed,  the  initial  change  has  been 
dilatation  caused  by  violent  and  sustained  effort,  such  as 
racing,  the  hypertrophy  being  secondary  to  this ;  but  even 
here  it  is  the  dilatation  and  not  the  compensatory  process 
which  has  to  be  considered. 

Causes  of  Hypeetrophy  of  the  Eight  Ventricle. 

Hypertrophy  of  the  right  ventricle,  as  of  the  left,  has 
its  most  common  cause  in  valvular  disease — in  this  instance 
chiefly  mitral  stenosis  or  insufficiency ; — and  after  valvular 
disease,  in  conditions  which  give  rise  to  obstruction  in  the 
pulmonary  circulation. 

Emphysema  and  bronchitis  are  the  lung  affections 
which  most  frequently  give  rise  to  hypertrophy  of  the 
right  ventricle,  but  the  hypertrophy  is  rarely  dissociated 
from  dilatation,  which  is  the  primary  effect  of  the  obstruc- 
tion in  the  pulmonary  capillaries.  Collapse  of  a  portion 
of  the  lungs,  contraction  of  a  lung  from  pleural  adhesions, 
fibroid  phthisis,  or  any  condition  which  throws  a  consider- 
able area  of  lung  surface  out  of  gear,  will  to  a  certain 
degree  give  rise  to  overwork  and  consequent  hypertrophy 
of  the  right  ventricle. 

Hypertrophy  of  the  Left  Ventricle.  Physical  Signs. 

The  Pulse. — The  pulse  will  be  that  of  the  condition  which 
has  given  rise  to  the  hypertrophy.  When  this  has  been 
high  arterial  tension  due  to  renal  disease,  gout,  lead  poison- 
ing, pregnancy,  etc.,  the  character  of  the  pulse  will  be  as 

T 


274  HEART  DISEASE. 

follows :  The  artery  will  be  full  between  the  beats,  will  not  be 
easily  flattened  under  the  fingers,  and  can  be  followed  some 
distance  up  the  forearm  like  a  cord.  The  pulse  wave  will 
not  have  a  violent  ictus,  but  will  rise  gradually  and  subside 
slowly,  and  as  it  makes  little  impression  on  the  fingers 
it  is  sometimes  described  as  weak,  but  when  the  attempt 
is  made  to  arrest  the  wave  very  firm  pressure  is  required. 
When  the  cause  of  the  hypertrophy  has  been  valvular 
disease,  the  character  of  the  pulse  will  be  as  described  in 
the  chapters  on  the  particular  lesion. 

The  Heart. — On  inspection,  there  may  or  may  not  be 
recognizable  bulging  over  the  cardiac  area ;  the  impulse  is 
not  extensive  or  violent  in  uncomplicated  cases;  the  ajDex 
beat,  if  visible,  is  seen  below  the  normal  point,  frequently 
in  the  sixth,  sometimes  even  in  the  seventh,  space,  and  is 
probably  also  displaced  somewhat  outwards ;  it  is  a  cir- 
cumscribed gentle  heave.  Occasionally  one  or  more  of 
the  intercostal  spaces  above  and  to  the  inner  side  of  the 
apex  line  may  be  seen  to  be  retracted,  but  this  is  very 
rare,  and  is  never  so  well  marked  in  hypertrophy  without 
valvular  disease  as  it  may  be  seen  in  aortic  regurgitation. 

By  palpation,  which  is  always  an  extremely  important 
part  of  the  physical  examination  of  the  heart,  the  apex 
beat  is  further  defined,  and  is  felt  as  a  powerful  but 
deliberate  thrust  in  the  space,  sometimes  distinctly  lifting 
the  adjacent  ribs.  The  more  the  fingers  are  pressed  into 
the  space,  the  more  distinctly  is  the  thrust  recognized. 
When  the  flat  of  the  hand  is  laid  over  the  cardiac  region, 
a  general  heaving  impulse  can  usually  be  felt,  but  when 
the  left  ventricle  is  alone  or  mainly  affected,  it  is  not  very 
conspicuous.  As  a  rule,  no  impulse  is  felt  to  the  right 
of  the  sternum  except  when  the  aorta  is  dilated,  in  which 
case  pulsation  may  be  felt  when  the  fingers  are  thrust  into 
the  second  and  third  spaces  near  the  sternum.  It  must 
be  added   that  sometimes  neither  apex  beat   nor  impulse 


HYPERTROPHY.  275 

can  be  seen  or  felt  when  the  hypertrophy  is  considerable. 
Mostly  this  is  in  deep-chested  individuals  with  large,  over- 
lapping lungs,  but  occasionally  hypertrophic  enlargement 
takes  a  direction  which  carries  the  heart  away  from  the 
chest  wall. 

Percussion  maps  out  more  or  less  accurately  the  enlarge- 
ment of  the  heart  downwards  and  to  the  left.  This 
demarcation  should  be  done  with  extreme  care,  but  it 
must  not  be  taken  for  granted  that  the  outline  drawn 
on  the  surface  corresponds  exactly  with  that  of  the  organ, 
or  gives  a  trustworthy  idea  of  its  size.  To  say  nothing 
of  the  difficulty  of  defining  deep  dulness,  the  heart  may 
enlarge  backwards  instead  of  laterally.  The  results  of 
percussion  must  be  correlated  with  all  the  other  evidence 
as  to  the  size  of  the  heart. 

Auscultation,  besides  teaching  the  character  and  in- 
tensity of  the  sounds,  must  be  made  to  contribute  to  the 
information  on  this  point  by  careful  noting  of  the  seat  of 
maximum  intensity  of  the  sounds  in  the  apex  region. 

The  left  ventricle  first  sound  as  heard  at  the  apex  is 
longer  and  of  lower  pitch  than  in  a  normal  state  of  the 
heart ;  either  the  mass  of  muscle  enters  into  contraction 
more  slowly,  and  the  muscular  tension  being  less  sudden 
yields  a  duller  sound,  or  the  thickness  of  the  walls  masks 
the  sound  produced  by  the  sudden  tension  of  the  valves  and 
tendinous  cords.  The  aortic  second  sound,  heard  at  the 
apex,  is  usually  louder  than  normal,  and  is  often  heard  at 
or  near  the  apex  more  distinctly  even  than  in  the  right 
second  space. 

The  systole  is  usually  somewhat  prolonged.  The  first 
sound  may  be  reduplicated,  due  to  the  two  first  sounds, 
produced  by  the  right  and  left  ventricles  respectively,  not 
coinciding.  This  indicates  that  the  left  ventricle  is  no 
longer  quite  equal  to  the  extra  work  imposed  upon  it,  and 
marks  the  supervention  of  a  tendency  to  dilatation. 


276  BE  ART  DISEASE. 

At  the  base  of  the  heart  the  left  ventricle  first  sound 
is  less  distinct  than  at  the  apex,  and  is  frequently  inaudible, 
while  the  accentuation  of  the  second  sound  is  rendered 
more  evident  by  the  absence  of  the  first.  When  this  sound 
is  not  only  accentuated  but  low-pitched  and  ringing,  it 
indicates  that  the  root  of  the  aorta  is  more  or  less  dilated, 
and  the  sound  will  be  heard  for  some  distance  to  the  right 
of  the  edge  of  the  sternum. 

The  sounds  of  the  right  ventricle  undergo  no  modifica- 
tion of  sufficient  importance  to  require  notice. 

Symptoms. 

Various  symptoms  are  described  as  resulting  from 
hypertrophy  of  the  heart — discomfort  from  the  violence 
of  the  impulse,  or  actual  pain  in  the  region  of  the  heart, 
tenderness  on  pressure  in  the  neighbourhood  of  the  apex, 
throbbing  sensations  in  the  head  and  neck,  pulsatile  noises 
in  the  ears,  or  audible  pulsation  in  the  carotid  and  other 
arteries.  The  action  of  the  heart  may  be  unduly  frequent, 
or  too  easily  excited,  or  abrupt  and  irritable,  or  irregular 
with  falterings  and  bounds,  which  are  very  disturbing  to 
the  subject,  and  the  heart  may  be  prone  to  palpitation. 
There  may  be  a  sense  of  respiratory  oppression,  with  sigh- 
ing and  desire  to  fill  the  chest  with  air. 

Some  of  the  symptoms  are  simply  the  result  of  the  size 
of  the  heart  and  of  the  vehemence  of  its  beat ;  others  are 
due,  not  to  the  hypertrophy  itself,  but  to  its  cause,  whether 
in  the  valves  or  in  the  vessels,  or  to  external  influences 
which  have  given  rise  to  it ;  others,  again,  are  common  to 
various  affections  of  the  heart,  functional  or  organic, 
besides  hypertrophy.  They  have  no  such  direct  or  definite 
bearing  on  prognosis  as  would  warrant  a  discussion  of  their 
significance,  though  a  sustained  frequency  of  the  pulse  is 
an  unfavourable  sign. 


hypertrophy.  277 

Prognosis. 

The  question  of  prognosis  in  relation  to  hypertrophy 
mostly  resolves  itself  into  this :  whether  the  compensation 
which  it  establishes  is  adequate  and  efficient,  and  how  far 
it  promises  to  be  durable.  The  danger  that  the  hyper- 
trophy may  go  beyond  the  requirements  of  the  occasion 
which  has  called  for  it  does  not,  in  my  opinion,  need 
consideration. 

Compensation  is  efficient  when  there  are  no  symptoms 
of  embarrassment  of  the  circulation,  and  when  the  heart 
responds  to  all  ordinary  calls  upon  it  without  undue  short- 
ness of  breath  or  respiratory  distress.  The  effects  of  exertion 
are  an  important  criterion,  due  allowance  being  made  for 
the  greater  liability  to  breathlessness  which  is  natural  to 
some  individuals,  or  is  produced  by  bodily  conformation  or 
which  results  from  a  sedentary  mode  of  life. 

But  the  sounds  of  the  heart  usually  give  notice  when 
it  is  overtaxed  by  the  resistance  to  the  onward  movement 
of  the  blood.  The  interval  between  the  first  and  second 
sound  may  be  prolonged,  the  systole  requiring  more  time 
than  under  ordinary  circumstances  to  complete  itself.  So 
long  as  the  normal  proportion  between  the  systolic  and 
diastolic  pauses  is  not  disturbed,  there  is  no  indication  that 
the  heart  is  unequal  to  its  work  or  is  suffering  from  the 
stress  put  upon  it :  but  when  the  systolic  interval  between 
the  first  and  second  sounds  is  lengthened  at  the  expense 
of  the  diastolic,  so  that  the  sounds  are  equidistant,  the 
period  of  repose  and  reconstitution  of  the  muscular  fibres 
of  the  ventricle  is  shortened,  and  their  nutrition  must  in 
time  suffer.  During  systole  the  blood  is  squeezed  out  of 
the  walls  of  the  heart,  and  it  is  during  the  diastolic 
relaxation  that  it  obtains  free  access  to  the  cardiac  fibres. 

Another  evidence  that  the  heart  is  yielding  to  the  strain 
of  overwork  is  reduplication  of  the  first  sound.     That  is, 


278  HEART  DISEASE. 

as  has  been  already  said,  due  to  want  of  synchronism 
between  the  two  ventricles  in  the  act  of  contraction,  or 
rather  in  arriving  at  that  point  in  their  contraction  when 
their  valves  and  tendinous  cords  and  muscular  walls  are  all 
made  tense.  This  reduplication  is  at  first  very  slight,  the 
two  sounds  are  separated  by  the  briefest  possible  interval, 
and  are  distinct  one  from  the  other  only  at  one  spot,  just 
to  the  inner  side  of  the  apex;  elsewhere  there  is  only  a 
slurring  or  prolongation  of  the  first  sound.  Later  the 
sounds  of  the  right  and  left  ventricles  are  quite  distinct, 
and  the  duplex  first  sound  is  recognized  over  a  considerable 
area,  usually  in  the  direction  of  the  ensiform  cartilage,  but 
sometimes  upwards.  One  variety  of  the  cantering  rhythm 
or  bruit  de  galop  is  produced  by  this  doubling  of  the  first 
sound,  where  the  successive  sounds  are  one-one,  two.  Some- 
times the  dislocation  of  the  ventricular  first  sound  is  so 
considerable  that  it  is  a  task  of  extreme  difficulty  to  identify 
the  sounds  of  the  heart  at  all,  and  associate  them  with  the 
systole  or  diastole  respectively  so  as  to  say  which  is  first 
and  which  second.  The  most  striking  and  confusing 
examples  are  met  with  in  aortic  stenosis  and  pericarditis. 
The  prognosis  becomes  serious  when  the  first  sound  is  broken 
up  in  any  considerable  degree. 

But  when  the  cardiac  hypertrophy  has  been  brought 
about  by  high  arterial  tension,  whether  associated  with 
renal  disease,  or  lead  poisoning,  or  other  cause,  there  must 
be  taken  into  consideration  the  possibility  that  the  power- 
ful heart  may  rupture  diseased  vessels  in  the  brain,  and 
if  the  arteries  are  conspicuously  degenerated  it  is  better 
for  the  patient  that  the  heart  also  should  undergo  some 
degree  of  degeneration;  and  sometimes  this  takes  place, 
so  that  the  patient  escapes  cerebral  haemorrhage,  and  lives 
longer,  though  he  succumbs  in  the  end  to  cardiac  failure. 


hypertrophy.  279 

'Treatment. 

Treatment  for  hypertrophy,  as  such,  appears  to  be 
out  of  place.  The  functional  vigour  and  energy  of  the 
overgrown  and  overstrong  heart  could  no  doubt  be  re- 
duced by  various  means — low  diet,  enforced  rest,  and 
such  drugs  as  aconite — but  unless  it  is  clear  that  the 
hypertrophy  has  gone  beyond  the  requirements  of  the 
condition  which  has  given  rise  to  it,  the  advantage  of  this 
procedure  would  be  more  than  doubtful.  Even  in  the 
attempt  to  relieve  the  incidents  of  hypertrophy,  palpita- 
tion, throbbing  sensations  in  the  chest,  prsecordial  oppres- 
sion, the  employment  of  direct  cardiac  depressants  is  rarely 
of  service,  and  is  at  times  attended  with  danger.  In  aortic 
stenosis,  for  example,  I  have  known  aconite,  given  with  a 
view  of  quieting  tumultuous  action  of  the  heart,  so  far 
reduce  the  contractile  energy  of  the  left  ventricle  that  it 
was  no  longer  able  to  cope  with  the  obstruction,  and  death 
quickly  followed  from  cardiac  asthenia,  the  pulse  becoming 
imperceptible,  the  extremities  livid,  and  the  surface  of 
the  body  cold  and  damp.  This  would  be  less  likely  to 
occur  where  the  cau3e  of  the  hypertrophy  was  obstruction 
in  the  peripheral  circulation,  as  the  arteries  and  capillaries 
are  relaxed  by  such  agents  as  depress  the  action  of  the 
heart. 

The  treatment  of  the  chief  causes  of  hypertrophy,  aortic 
disease  and  high  arterial  tension,  have  already  been  dis- 
cussed elsewhere,  so  that  what  we  have  to  consider  here  is 
not  the  treatment  of  hypertrophy  or  its  causes,  but  treat- 
ment suggested  by  the  hypertrophy.  We  shall  recognize, 
for  example,  the  necessity  of  diminishing  the  volume  and 
improving  the  quality  of  the  blood  by  appropriate  diet 
and  hygiene,  and,  if  necessary,  by  tonics.  We  shall  recog- 
nize, also,  the  desirability  of  diminishing  the  resistance  to 
the  onward  movement  of  the  blood  in  the  arterio-capillary 


280  HEAkT  DISEASE. 

network  by  care  in  diet  again,  by  aperients,  and  by 
eliminants  of  various  kinds.  In  some  cases,  the  resistance 
in  the  peripheral  circulation  may  be  further  lessened  with 
advantage  by  the  physiological  relaxants  of  the  arterioles 
and  capillaries,  such  as  nitroglycerine  and  the  nitrites.  By 
these  means  the  work  thrown  upon  the  heart  is  reduced, 
and,  if  necessary,  the  heart  may  be  strengthened  by  such 
remedies  as  strychnine  and  digitalis. 

All  these  measures  are  specially  required  when  the 
hypertrophy  is  no  longer  quite  equal  to  the  task  which  it 
had  originally  been  developed  to  perform,  and  reduplica- 
tion and  other  modifications  of  the  sounds  are  present. 
It  is  now  that  the  incidents  of  hypertrophy,  palpitation 
and  the  like,  are  most  commonly  complained  of,  and  they 
will  be  best  alleviated  or  removed  by  the  measures  just 
sketched,  by  relieving  the  heart  of  work  on  the  one  hand, 
and  by  helping  it  on  the  other. 


CHAPTER    XX. 
DILATATION. 

ETIOLOGY — VALVLLAR  DISEASE,  EXERTION,  STRAIN,  RENAL 
DISEASE,  ACUTE  BACTERIAL  INFECTIONS— PHYSICAL 
SIGNS— SYMPTOMS — PROGNOSIS — TREATMENT. 

The  word  "  dilatation  "  requires  no  explanation  as  applied 
to  the  cavities  of  the  heart.  Individual  cavities  may  be 
dilated,  as,  for  example,  the  left  auricle  in  mitral  stenosis 
or  regurgitation,  the  right  ventricle  in  pulmonary  emphy- 
sema or  mitral  disease ;  but  when  spoken  of  as  a  form  of 
heart  disease,  dilatation  usually  means  dilatation  of  the 
left  ventricle,  mostly  with,  but  sometimes  without,  dilata- 
tion of  the  right  ventricle.  Together  with  the  expansion 
of  the  cavity  of  the  ventricle  there  may  be  more  or  less 
thickening  of  its  walls,  representing  an  attempt  at  hyper- 
trophy, compensatory  of  the  dilatation  itself,  or  of  the 
difficulty  in  the  circulation  which  has  led  to  it.  The  walls 
of  the  heart  may  have  an  approximately  normal  thickness, 
which  will  really  imply  a  certain  degree  of  hypertrophy, 
or  they  may  be  distinctly  thinned.  The  parietes  may  have 
a  normal  colour,  consistence,  and  structure,  or  they  may 
be  pale,  flabby,  and  degenerated,  or  dense  and  tough  from 
fibroid  substitution.  But  even  more  important  than  the 
anatomical  condition  is  the  physiological  or  functional 
condition,  the  special  characteristic  of  which  is  that  the 
ventricle  does  not  complete  its  systole,  but  only  expels  a 
portion  of  its  contents. 


282  HEART  DISEASE. 

Dilatation  of  the  heart  may  be  contrasted  with  hyper- 
trophy rather  than  compared  with  it.  Hypertrophy  is 
compensatory  and  an  evidence  of  vigour ;  dilatation  is,  for 
the  most  part,  a  confession  of  failure  on  the  part  of  the 
heart  muscle  and  an  aggravation  of  other  causes  of  inter- 
ference with  the  circulation  which  may  be  in  operation. 
In  hypertrophy  the  augmented  mass  and  increased  strength 
of  the  muscular  walls  enable  the  ventricles  to  complete 
their  contraction  in  the  face  of  difficulty.  The  result  of 
dilatation  is  that  the  ventricles  habitually  fail  to  expel 
the  whole  of  their  contents.  Very  frequently  it  is  only  a 
very  small  proportion  of  the  blood  which  is  projected  into 
the  great  arteries.  In  well-marked  cases  the  chambers  of 
the  heart  are  always  full,  and  little  blood  being  received 
and  expelled,  there  is  a  stagnation  in  the  auricles  and 
ventricles.  It  has  seemed  to  me  that  the  imperfect  empty- 
ing of  the  ventricles  has  not  always  been  fully  realized  as 
the  special  feature  of  dilatation,  but  it  will  be  seen  that  if 
a  dilated  ventricle  launched  the  whole  of  its  contents  into 
the  arterial  circulation,  the  amount  being  much  larger,  the 
rate  of  movement  of  blood  would  be  greatly  accelerated, 
whereas  the  contrary  is  the  case. 

A  distinction  must  be  drawn  between  the  dilatation 
due  to  inherent  weakness  of  the  muscular  walls  of  the 
heart  and  that  attending  valvular  disease. 

Etiology. 

Valvular  Disease. — The  dilatation  attending  aortic  re- 
gurgitation belongs  to  a  different  category  from  primary 
dilatation,  as  has  already  been  shown,  and,  instead  of 
aggravating  the  difficulties  of  the  circulation,  it  is  a  part 
of  the  compensatory  arrangement.  It  is  clear  that  if  a 
certain  proportion  of  the  blood  projected  into  the  aorta  at 
each  systole  returns  to  the  ventricle  during  diastole,  it  is 


DILATATION.  283 

an  advantage,  and  indeed  a  necessity,  that  the  capacity  of 
the  ventricle  should  be  increased,  so  that,  in  spite  of  the 
reflux,  a  normal  amount  of  blood  may  remain  in  the  arteries 
and  be  distributed  to  the  tissues.  The  dilatation,  however, 
in  aortic  regurgitation  is  accompanied  by  hypertrophy 
which  enables  the  ventricle  to  contract  perfectly,  so  that 
the  characteristic  of  dilatation — the  partial  and  imperfect 
emptying  of  the  ventricle — is  not  present. 

It  is  probable,  again,  that  the  dilatation  of  the  left  ven- 
tricle met  with  in  mitral  regurgitation  may  have  a  similar 
compensatory  effect.  It  would  seem  to  be  an  advantage, 
since  some  of  the  blood  regurgitates  into  the  auricle,  that 
the  ventricle  should  contain  sufficient  to  allow  for  this,  and 
yet  discharge  a  due  amount  into  the  aorta.  In  dilatation  con- 
secutive to  mitral  regurgitation,  moreover,  there  is  a  certain 
degree  of  hypertrophy,  and  the  systole  is  carried  through. 
The  dilatation  of  mitral  regurgitation  stands,  then,  on  a 
totally  different  footing  from  primary  dilatation. 

The  mode  of  production  of  dilatation  of  the  heart  is 
highly  complex ;  it  is  usually  understood  to  be  the  result 
of  a  gradual  yielding  of  the  walls  of  the  ventricles,  either 
from  their  own  inherent  weakness  or  from  undue  resistance 
to  the  onward  course  of  the  blood.  It  is  often  supposed  also, 
when  dilatation  exists,  that  it  is  an  established  and  more  or 
less  unvarying  or  progressive  condition.  Both  these  ideas 
require  modification. 

Exertion. — All  violent  or  protracted  exertion  is  attended 
with  temporary  dilatation  of  the  heart,  which  may  go  so  far, 
even  in  strong  and  healthy  persons,  as  to  give  rise  to  tempo- 
rary murmurs.  Loud  murmurs  so  produced  may  be  heard  at 
the  apex,  over  the  tricuspid  area  and  over  the  pulmonic  area, 
in  individuals  who  have  no  evidence  of  cardiac  weakness 
at  the  time,  and  who  develop  no  valvular  or  other  cardiac 
disease  for  many  years  afterwards.  A  personal  friend  always 
had  a  loud,  systolic,  pulmonic  murmur  after  hunting,  which 


284  HEART  DISEASE. 

sometimes,  when  there  had  been  a  severe  run,  lasted  two  or 
three  days.  It  is,  again,  not  very  uncommon  for  young  and 
strong  men  to  return  from  climbing  in  Switzerland  with 
more  or  less  dilatation  of  the  heart,  which  may  persist  for 
weeks.  This  is  usually  when  little  exercise  has  been  taken 
during  the  year,  and  considerable  ascents  or  very  long 
walking  excursions  have  been  made  without  sufficient 
preliminary  training.  Boat-races  no  doubt  give  rise  to 
temporary  dilatation,  and  it  may  be  met  with  as  a  result  of 
training  for  races.  It  might,  perhaps,  be  better  to  speak  of 
distension  of  the  cavities  of  the  heart  in  these  instances, 
rather  than  of  dilatation. 

In  violent  exercise  the  pulse  in  becoming  extremely 
frequent  also  becomes  extremely  soft  and  short;  the 
arterioles  and  capillaries  are  relaxed  in  order  to  facilitate 
the  rapid  movement  of  the  blood  which  is  necessary  to 
supply  fuel  and  oxygen  to  the  muscles  during  exertion,  and 
the  arterial  tension  is  low.  The  resistance  to  be  overcome 
by  the  ventricles  is  thus  reduced  to  a  minimum,  which 
diminishes  the  liability  to  over-distension. 

But  the  circumstances  which  are  capable  of  producing 
a  temporary  distension  of  the  ventricles  in  a  sound  and 
vigorous  state  of  the  organ  will  be  competent  to  give  rise  to 
dilatation  when  it  is  weak  and  flabby,  and  when  other 
conditions  are  present  which  tend  to  dilatation,  and  it  is 
more  likely  that  the  weakly  ventricles  give  way  from  time 
to  time  under  stress  and  fail  to  recover  perfectly,  than  that 
the  yielding  is  gradual  and  continuous. 

Overstrain  and  Degenerative  Change.  —Acute  dilatation  of 
the  heart  is  more  common  than  is  generally  supposed. 

In  a  very  large  proportion  of  the  cases  admitted  into 
hospital  suffering  from  symptoms  due  to  cardiac  dilatation, 
there  has  been  an  acute  aggravation  of  the  affection  from 
work  or  exposure,  and  under  treatment  a  considerable  dimi- 
nution in  the  size  and  capacity  of  the  heart  is  commonly 


DILATATION.  285 

observed.  But  cases  occur  in  which  there  is  ground  for 
supposing  that  dilatation  has  been  induced  at  once  in  a 
heart  not  previously  affected.  The  following  are  examples 
selected  as  illustrations. 

A  gentleman  at  the  age  of  70,  in  vigorous  health  and 
capable  of  any  ordinary  amount  of  exercise,  overtook  a 
labourer  pushing  a  heavily  laden  wheelbarrow  uphill,  who 
had  to  stop  and  rest  every  few  yards.  Proud  of  his  strength, 
he  told  the  man  to  stand  aside,  and  himself  wheeled  the 
barrow  for  some  distance  at  a  good  pace.  He  lost  his  breath 
and  found  that  he  did  not  recover  it  as  he  expected,  but 
that  he  continued  to  pant  and  to  be  conscious  of  violent 
action  of  the  heart,  accompanied  by  a  sense  of  oppression  in 
the  chest.  He  got  home  with  difficulty,  the  least  exertion 
was  attended  with  shortness  of  breath,  and  he  could  not 
rest  at  night.  After  a  few  days  he  sent  for  his  medical  man, 
when  the  physical  signs  of  dilatation  of  the  heart  were  found 
to  be  present.  Mitral  insufficiency  was  quickly  established, 
and  when  I  saw  him  considerable  dropsy  existed.  He  died 
shortly  afterwards. 

A  gentleman,  aged  about  55,  remarkably  strong  and 
active,  who  was  said  to  have  had  a  slight  attack  of  pleurisy 
shortly  before,  ran  quickly  up  a  long  flight  of  stairs  in  the 
City.  On  arriving  at  the  top  he  was  found  gasping  for 
breath,  unable  to  speak  and  scarcely  able  to  stand.  He  was 
soon  sufficiently  recovered  to  be  sent  home,  and  a  few  days 
later  he  was  brought  by  his  medical  attendant  to  my  con- 
sulting-room, chiefly  in  order  that  I  might  aid  in  enforcing 
the  rest  and  care  which  were  considered  necessary.  The 
patient  admitted  that  he  was  weak  and  soon  out  of  breath, 
but  declared  that  he  was  quite  equal  to  business.  The 
pulse  was  irregular  in  force  and  frequency,  the  apex  beat  of 
the  heart  diffuse,  devoid  of  the  impulse  or  thrust,  and  dis- 
placed downwards  to  the  sixth  space  and  outwards  beyond 
the  nipple  line,  and  the  other  physical  signs  of  a  considerable 


286  HEART  DISEASE. 

degree  of  dilatation  were  present.  With  great  reluctance 
a  certain  amount  of  rest  and  treatment  was  submitted  to, 
and  the  heart  and  pulse  became  stronger  and  steadier,  and 
the  apex  beat  came  in  towards  its  normal  situation  about  an 
inch. 

Two  months  later  the  patient  ran  down  from  a  committee- 
room  in  the  House  of  Commons  for  a  bag  of  papers  which  he 
had  forgotten,  and  back  again.  An  attack  of  the  same  kind 
as  that  just  described  came  on,  and  this  time  lasted  longer. 
The  evidences  of  dilatation  of  the  left  ventricle  were  more 
marked,  and  oedema  of  the  ankles  soon  came  on.  The 
patient  was  kept  in  his  room,  and  as  far  as  practicable 
at  rest  in  bed  or  on  a  couch.  Improvement  was  again 
obtained,  but  much  more  slowly  than  before,  and  as  my 
visits  were  the  chief  restraint  upon  him,  after  a  brief 
attendance  at  short  intervals,  further  consultations  were 
put  off  indefinitely. 

Within  a  few  days  the  exertion  of  going  downstairs  and  a 
serious  imprudence  in  diet  brought  on  a  return  of  symptoms, 
and  the  osdema  of  the  lower  extremities  was  shortly  compli- 
cated by  thrombosis  of  the  deep  femoral  vein  of  the  left  side, 
which  extended  along  the  iliac  vein  to  the  vena  cava  and 
down  the  right  iliac  and  femoral  veins.  A  tedious  illness 
followed,  which  finally  proved  fatal  by  extension  of  the 
thrombosis  to  the  renal  veins,  the  heart  itself  appearing  to 
improve  somewhat. 

Another  case  was  that  of  a  boy  who  was  admitted  into 
St.  Mary's  Hospital  with  extreme  dilatation  of  both  ven- 
tricles. He  had  had  no  previous  illness,  but  had  been 
underfed.  Most  Londoners  will  be  familiar  with  the  ap- 
pearance of  lads  in  the  scanty  attire  of  the  cinder-path,  who 
are  making  use  of  the  streets  as  a  training-ground  for 
races,  usually  in  the  dusk  of  the  evening,  after  working 
hours  ;  perhaps,  also,  this  time  is  chosen  to  avoid  police 
interference.     I  have  myself  often  been  astonished  at  the 


DILATATION.  2S7 

pace  and  endurance  of  these  athletes-under-difficulties.  The 
patient  had  been  training  in  this  way,  and  had  persevered  in 
spite  of  shortness  of  breath,  till  severe  symptoms  set  in.  He 
died  soon  after  admission,  and  the  ventricles  were  found  to 
be  enormously  dilated. 

Renal  Disease. — A  certain  degree  of  dilatation  of  the  left 
ventricle  usually  occurs  at  the  onset  of  acute  renal  disease, 
under  the  combined  influence  of  the  resistance  in  the 
peripheral  circulation  and  of  the  enfeeblement  of  the  heart. 

It  is  very  striking  in  watching  the  course  of  a  case  of 
what  is  commonly  termed  "large  white  kidney,"  in  which 
the  patient  survives  the  dropsical  stage  and  the  kidney 
tends  to  approximate  that  of  the  "  contracted  granular." 
At  the  outset  the  heart  is  greatly  dilated,  the  apex  beat  is 
not  palpable,  and  the  first  sound  is  short  and  feeble.  The 
pulse  is  only  of  moderate  tension,  as  there  is  little  force  in 
the  cardiac  systole.  After  the  lapse  of  about  six  months  the 
dropsy  may  all  subside,  and  the  pulse  will  then  be  found  to 
be  one  of  higher  tension  with  the  vessel  in  a  state  of 
hypertonias.  The  heart  will  have,  to  a  great  extent,  re- 
covered from  its  dilatation,  and  will  have  undergone  very 
marked  hypertrophy,  and  the  apex  beat  will  be  easily  felt 
and  forcible.  The  patient  will  then  be  liable  to  die  from 
ursemic  convulsions  as  in  chronic  interstitial  nephritis. 

In  cases  which  are  from  the  outset  of  the  type  of 
"  granular  kidney,"  associated  with  very  high  arterial 
tension,  dilatation  of  the  heart  is  seldom  met  with,  though 
the  hypertrophy  of  the  left  ventricle  is  often  enormous. 
This  is  what  one  would  expect,  as  here  the  increase  of  the 
peripheral  resistance  and  of  the  strain  on  the  heart  is 
gradual,  so  that  the  heart  has  time  to  hypertrophy,  to 
cope  with  the  extra  work  thrown  on  it,  whereas  in  acute 
nephritis  a  severe  strain  is  suddenly  put  upon  it  which  it  is 
unable  to  meet,  and  thus  dilatation  of  the  left  ventricle 
occurs. 


288  HEART  DISEASE. 

Acute  Bacterial  Infections. — In  acute  rheumatism  and 
chorea  there  is  usually  a  certain  degree  of  cardiac  dila- 
tation, which  is  often  extreme  in  cases  of  acute  pericarditis. 
Attention  has  been  called  to  this  in  the  chapter  on  peri- 
carditis, so  it  will  not  be  further  discussed  here.  In  pneu- 
monia the  right  ventricle  is  especially  liable  to  become 
dilated  under  the  combined  effects  of  the  extra  strain 
thrown  on  it  by  the  obstruction  to  the  flow  of  blood  through 
the  lungs  and  the  damage  to  the  cardiac  muscle  by  the 
action  of  the  bacterial  toxins. 

Influenza  is  a  common  cause  of  cardiac  dilatation  which 
is  liable  to  be  overlooked  and  to  be  a  source  of  trouble  after 
the  acute  illness  has  subsided,  as  the  patient  is  apt  to  go 
about  and  resume  his  ordinary  avocations  too  soon  after 
the  attack,  and  increase  or  perpetuate  the  dilatation. 

Undue  exertion  at  an  early  period  after  any  acute 
bacterial  infection,  e.g.  enteric  fever,  is  liable  to  induce 
cardiac  dilatation,  as  the  heart  muscle  will  have  suffered 
a  varying  degree  of  injury  from  the  toxins  evolved  by  the 
micro-organisms,  and  will  not  be  able  to  stand  any  extra 
strain,  even  if  it  has  not  given  out  during  the  illness  itself. 

Psychological  Influences. — Another  cause  of  dilatation  of 
the  heart  is  anxiety.  The  influence  of  prolonged  mental 
depression  upon  the  heart,  as  experienced  by  the  sensation 
of  aching,  oppression,  and  weight  which  attends  grief  and 
anxiety,  which  were  considered  to  point  to  the  heart  as  the 
seat  of  emotion  generally,  is  indicative  of  an  injurious  effect 
upon  this  organ.  The  combination  of  overwork,  excitement, 
worry,  and  trouble,  often  met  with  in  City  life,  esjDecially 
on  the  Stock  Exchange  or  in  mercantile  or  financial  circles 
during  a  commercial  or  financial  crisis,  is  responsible  for 
many  cases  of  cardiac  dilatation  among  men,  and  domestic 
anxieties — grief  on  account  of  children  who  have  died  or 
given  trouble,  etc., — may  have  the  same  effect  among 
women. 


DILATATIOX.  289 

Injudicious  Regime. — Among  the  special  causes  of  dila- 
tation of  the  heart — acting,  no  doubt,  on  pre-existing 
tendencies — which  have  come  under  my  notice,  are  inju- 
dicious hydropathic  treatment,  the  so-called  Banting  method 
of  reducing  obesity,  and  inhalation  of  the  fumes  of  Himrod's 
powder  for  the  relief  of  asthma. 

In  one  case  a  gentleman  suffering  from  dyspeptic 
symptoms,  probably  due  to  cardiac  weakness  and  consequent 
sluggish  circulation  in  the  abdominal  viscera,  underwent  a 
routine  treatment  by  baths,  wet  cold  packs,  and  compresses, 
under  which  attacks  of  dyspnoea  came  on  and  oedema  set 
in.  He  had  previously  been  under  the  care  of  competent 
observers,  who  had  not  found  any  serious  degree  of  dilata- 
tion. The  dropsy  advanced  in  spite  of  treatment,  and  when 
I  saw  the  patient  it  was  considerable,  and  the  physical 
signs  gave  evidence  of  extreme  dilatation  and  thinning  of 
the  left  ventricle.  Death  occurred  suddenly  during  a 
paroxysm  of  dyspnoea. 

Another  patient  came  straight  to  my  consulting-room 
from  a  hydropathic  institution,  where  he  had  undergone 
vigorous  treatment  for  digestive  and  liver  derangements, 
attributed  to  long  residence  in  India.  He  was  very  anaBinic, 
and  breathless  ;  the  heart  was  greatly  dilated  and  its  action 
irregular,  and  there  was  incipient  oedema.  Fortunately  he 
recovered. 

One  of  the  most  extreme  cases  of  dilatation  I  have  ever 
met  with  was  in  the  case  of  a  lady  who  had  undergone  an 
amateur  course  of  Banting  treatment  for  obesity.  She  had 
lost  some  of  her  fat,  but  had  become  extremely  breathless, 
so  that  to  walk  across  a  room  or  put  on  an  article  of 
clothing  with  the  assistance  of  her  maid  caused  her  to  pant 
and  gasp  for  breath  in  a  very  painful  way.  The  pulse  was 
weak,  small,  and  very  irregular;  no  impulse  or  apex  beat 
could  be  felt,  and  the  size  of  the  heart,  as  mapped  out 
according  to  the  deep  dulness,  was  incredibly  large,  had  not 

u 


290  HEART  DISEASE. 

the  results  of  percussion  been  confirmed  by  the  sounds 
being  audible  over  the  entire  area  of  dulness,  and,  later,  by 
a  feeble  apex  beat  in  the  seventh  space  near  the  mid-axillary 
line.  Apparently  habitual  high  arterial  tension  had  been 
exaggerated  by  an  exclusively  nitrogenous  diet,  and,  under 
it,  the  ventricle  had  given  way. 

It  may,  perhaps,  be  well  to  add  that  in  the  treatment  of 
obesity  by  beefsteak  and  copious  draughts  of  hot  water 
there  has  not  been,  according  to  my  experience,  increase  of 
arterial  tension,  but  the  reverse. 

The  following  case  is  the  most  serious  of  several  attribu- 
table to  Himrod's  powder : — 

In  December,  1883,  I  saw,  with  Dr.  Andrews,  of  Hamp- 
stead,  a  gentleman,  aged  about  thirty-six,  apparently  of 
sturdy  constitution,  who,  after  an  attack  of  bronchitis, 
suffered  from  severe  nocturnal  attacks  of  asthmatic  dyspnoea. 
A  month  at  Hastings  had  apparently  restored  his  health ; 
but,  after  a  fortnight  of  work  in  London,  his  nocturnal 
asthma  and  shortness  of  breath  were  as  bad  as  ever.  For 
the  asthmatic  attacks  he  had  inhaled  immoderately  the 
fumes  of  Himrod's  powder,  obtaining  relief  for  the  time, 
but  with  disastrous  after-effects.  The  whole  house  was 
reeking  with  the  odour  of  the  fumes  at  the  time  of  our 
consultation.  Dr.  Andrews  had  witnessed  the  rapid  develop- 
ment of  the  condition  of  the  heart  which  existed.  The 
area  of  cardiac  dulness  was  greatly  increased ;  no  apex  beat 
was  recognizable  ;  there  was  a  doubtful  systolic  murmur 
(mitral)  in  the  region  of  the  apex,  a  loud  systolic  murmur 
(tricuspid)  near  the  ensiform  cartilage,  and  a  faint  systolic 
aortic  murmur.  Tricuspid  incompetence  was  further  dis- 
tinctly manifested  by  great  enlargement  of  the  liver,  and 
by  marked  jugular  pulsation.  There  was  nothing  in  the 
patient's  habits,  or  mode  of  life,  or  previous  history  which 
was  at  all  calculated  to  give  rise  to  dilatation  of  the  heart, 
and   I   had   the   less   hesitation    in   attributing   it   to   the 


DILATATION.  291 

solanaceous  fuines,  from  having  seen  similar  effects  in  other 
cases.  In  about  a  fortnight,  after  free  purgation  by  calomel 
and  the  administration  of  digitalis,  the  patient  was  much 
better,  free  from  asthma,  and  able  to  walk  upstairs,  while 
the  liver  had  gone  down  to  its  usual  size.  The  heart 
remained  very  large,  gave  no  defined  apex  beat  and  only 
a  diffuse  general  impulse,  while  a  high-pitched  mitral 
murmur,  a  louder  tricuspid  murmur  of  low  pitch,  and  a 
faint  aortic  murmur,  all  systolic,  were  audible.  The  action 
of  the  heart  was  curious ;  now  and  then  there  was  a  sudden 
bump  against  the  palm  of  the  hand  placed  over  the  right 
ventricle,  and  it  was  found  that  the  beats  of  the  heart  were 
in  pairs,  only  the  first  of  which  was  accompanied  by  a 
systolic  apex  murmur,  the  second  having  a  loud  first  and 
second  sound,  but  scarcely  reaching  the  pulse.  With 
both  beats  the  loud  tricuspid  murmur  was  present.  The 
improvement  continued,  so  that  the  patient  resumed  his 
duties  before  the  end  of  January,  and  attended  regularly  to 
business  through  the  month  of  February.  In  March  came 
another  relapse  which  led  to  dropsy,  and  the  patient  died 
early  in  April.  Fortunately  an  examination  of  the  body 
was  permitted,  notes  of  which  are  as  follows  : — 

There  was  much  oedema  of  the  legs  and  right  arm, 
but  no  fluid  in  the  abdomen.  The  heart  was  enormous, 
measuring  six  inches  and  a  half  from  base  to  apex,  and 
sixteen  and  a  half  in  circumference.  It  was  flabby, 
pale,  fatty  looking,  not  lacerable.  The  right  auricle  was 
greatly  dilated  and  very  thin,  the  wall  being  translucent 
at  one  part ;  the  appendix  was  filled  up  by  solid  clot  and 
stained  black  by  blood.  The  tricuspid  orifice  took  four 
fingers  easily ;  there  was  no  roughness.  The  right  ventricle 
was  enormously  dilated,  and  would  almost  have  held  a 
duck's  egg ;  the  walls  were  thin,  soft,  and  flabby,  the  valve 
stained  black ;  the  flaps  were  thin  and  the  cords  delicate. 
The  pulmonary  artery  and  valves  were  normal.     The  left 


292  HEART  DISEASE. 

auricle  was  not  at  all  dilated,  the  appendix  contrasting  with 
the  right,  and  compared  with  the  other  cavities  curiously 
small.  The  mitral  orifice  would  admit  two  fingers.  The 
left  ventricle,  like  the  right,  was  enormously  dilated,  and 
looked  as  if  it  would  hold  a  fist :  the  walls  were  thin, 
mottled,  and  flabby,  but  not  lacerable ;  the  papillary 
muscles  were  small,  the  mitral  valve  and  cords  quite 
normal,  and  remarkably  free  from  thickening.  The  aorta 
was  very  small  and  the  valves  normal. 


Physical  Signs. 

The  pulse  in  advanced  dilatation  of  the  heart  is  usually 
irregular  in  rhythm  and  unequal  in  force  of  beat,  and  is 
sudden,  short,  unsustained,  and  usually  easily  compressed. 
The  artery  at  the  wrist  may  be  large  or  small ;  it  will  be 
specially  large  when  there  has  been  antecedent  high  tension 
which  has  dilated  the  arteries.  The  significance  of  a  pulse 
of  this  character  is  not  absolute,  as  all  these  characters  may 
be  present  when  there  is  no  recognizable  change  in  the 
walls,  cavities,  or  valves  of  the  heart,  apparently  from 
disordered  nervous  influence  only.  The  pulse,  again,  need 
not  be  irregular  in  advanced  dilatation  of  the  heart  so  long 
as  the  patient  is  in  repose  and  the  breathing  is  tranquil 
and  easy.  The  regularity,  however,  is  easily  disturbed  by 
exertion  or  effort,  or  by  bronchitis,  or  merely  by  deep 
breathing.  In  moderate  and  slight  dilatation  the  pulse 
may  be  regular,  but,  while  irregularity  is  the  rule,  there  is 
no  such  constant  relation  between  the  degree  of  regularity 
or  irregularity  of  the  pulse  and  the  amount  of  dilatation  of 
the  heart  as  to  make  one  diagnostic  of  the  other. 

The  Heart. — In  the  examination  of  the  heart,  inspection 
and  particularly  palpation  will  be  of  the  greatest  importance. 
The  visual  examination  will  be  directed  to  the  situation  and 
character  of  the  apex  beat  and  to  the  impulse  of  the  right 


DILATATION.  293 

ventricle.  Retraction  or  bulging  of  the  intercostal  spaces, 
elsewhere  than  at  the  visible  apex  beat,  will  be  noted. 

The  apex  will  be  displaced  outwards  and  downwards, 
and  it  may  be  visible  over  a  large  area.  Very  commonly  it 
cannot  be  seen  at  all,  and  the  point  of  maximum  apparent 
impulse  does  not  necessarily  belong  to  the  true  apex.  The 
right  ventricle  impulse  will  be  diffuse,  if  recognizable  at  all, 
and  as  a  rule  it  is  inconspicuous. 

Palpation  in  most  cases  of  dilatation  furnishes  informa- 
tion which  contributes  more  to  precision  of  idea  as  to  the 
actual  state  of  the  heart  than  any  other  branch  of  physical 
exploration.  The  right  hand  should  be  applied  closely 
over  the  entire  cardiac  region,  the  palm  over  the  right 
ventricle,  the  fingers,  spread  out  and  close  together  alter- 
nately, over  the  apex  region.  Distinct  impulse  over  the 
right  ventricle,  while  it  indicates  more  or  less  obstruction 
in  the  pulmonary  circulation,  indicates  also  some  degree 
of  vigour  in  this  ventricle  available  for  compensatory 
work.  A  mere  vibration  has  a  converse  significance.  The 
first  object  of  attention,  however,  will  be  the  identification 
of  the  point  of  maximum  impulse  in  the  apex  region,  and 
a  careful  estimation  of  the  area  over  Avhich  the  apex  beat 
extends,  and  of  its  force  and  character ;  whether,  for 
example,  it  is  a  mere  concussion  of  the  chest  wall  or  a 
more  or  less  distinct  thrust  at  any  point.  Sometimes  the 
word  "slapping"  is  employed  to  describe  the  impulse  or 
apex  beat  characteristic  of  dilatation.  Further  exploration 
will  be  made  by  pressing  the  fingers  into  the  intercostal 
spaces  around  and  beyond  the  point  of  maximum  impulse, 
and  it  must  be  borne  in  mind  that  this  impulse  may  not 
be  the  real  apex  beat,  but  the  impulse  of  the  right 
ventricle.  Sometimes  impulse  is  detected  much  above  the 
normal  situation,  in  the  fourth  space  perhaps  as  far 
outwards  as  the  anterior  axillary  fold  or  behind  it,  or  it 
may  be  concealed  by  the  female  mamma.     It  may  be  the 


294  HEART  DISEASE. 

left  edge  of  the  right  ventricle  resting  on  the  inter- 
ventricular septum  which  is  here  felt,  or  a  part  of  the 
rounded  apex  of  the  left  ventricle.  According  as  the  apex 
is  capable  of  giving  a  distinct  thrust  or  communicates  only 
a  diffuse  shock,  and,  according  as  the  beat  is  well-defined 
and  steady,  or  vaguely  felt  over  a  considerable  area,  will 
be  the  estimate  of  the  degree  of  dilatation  and  of  the 
thickness  or  thinness  of  the  heart  wall.  Not  unfrequently 
neither  impulse  nor  apex  beat  can  be  detected,  or  the 
impulse  is  so  vague  that  it  cannot  be  localized ;  unless 
this  is  due  to  overlapping  lung,  it  indicates  great  weakness 
of  the  muscular  walls  of  the  heart. 

By  deep  percussion  the  outline  of  the  heart  can  be 
more  or  less  accurately  mapped  out.  It  is  more  rounded 
in  the  apex  region  than  normal,  and  the  area  of  dulness 
is  greatly  extended  to  the  left.  When  no  impulse  of  any 
kind  can  be  felt  we  may  have  to  depend  entirely  on 
percussion  for  information  as  to  the  size  of  the  heart.  I 
have  found  continuous  deep  dulness  outwards  as  far  as 
the  mid-axillary  line  and  downwards  to  the  seventh  space, 
shown  to  be  cardiac  by  the  intensity  of  the  sounds  at 
the  extreme  limits,  and,  when  the  heart  had  gained  strength, 
by  an  apex  beat  recognizable  by  palpation  at  the  farthest 
point. 

Auscultation. — The  characteristic  modification  of  the 
sounds  of  the  heart  produced  by  dilatation  is  that  the  left 
ventricle  first  sound  becomes  short ;  usually  it  is  also 
sharper  than  normal.  Probably  from  this  change  in  the 
character  of  the  left  ventricle  first  sound  it  is  almost 
always  audible  in  the  aortic  area,  contrasting  in  this 
respect  with  hypertrophy.  It  is  audible  also  to  the  left  of 
the  apex  beat.  When  no  impulse  or  apex  beat  can  be 
felt,  the  sounds,  and  especially  the  first,  must  be  made 
use  of  to  ascertain  how  far  to  the  left,  the  left  border 
and  apex  of  the  heart  have  been  carried  by  the  dilatation, 


DILATATION'. 


295 


and  in  what  degree  the  enlargement  is  due  to  dilatation 
or  hypertrophy.  Percussion,  of  course,  maps  out  the  deep 
dulness,  and  shows  approximately  the  limit  of  the  heart 
and  its  extension  to  the  left,  but  the  point  of  maximum 
intensity  of  the  sounds  and  the  area  over  which  they  are 
audible  will  corroborate  or  correct  the  idea  formed  as  to 
the  size  of  the  heart  from  percussion,  and  percussion  yields 
no  information  whatever  as  to  the  kind  of  enlargement,  but 
leaves  it  to  be  supplied  by  the  character  of  the  sounds  on 
auscultation. 

Not  uncommonly  dilatation  of  the  left  ventricle  gives 
rise  to  a  systolic  apex  murmur,  obviously  due  to  mitral 
incompetence.  This  is  induced  by  imperfect  accomplish- 
ment of  the  constriction  of  the  orifice,  which  is  part  of  the 
normal  contraction  of  the  ventricle,  and  which  co-operates 
with  the  curtains  of  the  valves  in  preventing  regurgitation 
into  the  auricle.  Mitral  valvular  disease  is  attended  with 
precisely  the  same  combination  of  conditions — incompe- 
tence of  the  valve  and  dilatation  of  the  ventricle — and 
of  physical  signs — a  systolic  murmur  and  displacement  of 
the  apex  beat  with  increased  cardiac  dulness.  The  prog- 
nosis is  different  in  the  two  cases,  and  it  is  therefore 
important  to  distinguish  between  them.  This  cannot 
always  be  done  by  means  of  physical  signs  alone,  but  they 
may  give  important  information. 

The  presence  of  the  left  ventricle  first  sound  and  its 
peculiar  character  in  primary  dilatation,  and  its  partial  or 
complete  replacement  by  the  murmur  in  a  valve  lesion  will 
sometimes  be  of  service  in  differential  diagnosis.  The 
age  of  the  patient,  and  the  history  of  the  case,  will  be  of 
great  help,  and  the  mode  of  onset  of  the  symptoms  and 
their  causation  should  be  carefully  inquired  into.  If  the 
patient  is  middle-aged  and  the  symptoms  date  from  some 
imprudent  over-exertion,  the  presumption  will  be  in  favour 
of  primary   dilatation.      If  there    is    a    history    of   acute 


296  HEART  DISEASE. 

rheumatism,  there  will  be  little  doubt  as  to  the  diagnosis, 
especially  if  the  patient  be  a  child  or  young  adolescent, 
and  there  is  evidence  of  compensatory  hypertrophy  of  the 
right  ventricle. 

There  is  nothing  in  dilatation  of  the  cavities  of  the 
heart  to  affect  specially  and  directly  the  second  sound,  but, 
in  proportion  as  this  condition  of  the  ventricles  impairs 
the  propulsive  energy  of  the  systole  the  second  sound  will 
be  enfeebled,  and  the  aortic  second  sound  is  usually  weak 
as  compared  with  the  left  ventricle  first  sound.  The 
relative  loudness  of  the  sounds  therefore  enters  into  the 
considerations  from  which  may  be  calculated  the  efficiency 
of  the  ventricle. 

Very  important  information  is  often  supplied  by 
observation  of  the  intervals  between  the  first  and  second 
and  the  second  and  first  sounds,  the  short  and  long  pauses 
respectively.  When,  with  dilatation  of  the  left  ventricle 
there  is  resistance  in  the  arterioles  and  capillaries,  which 
is  very  commonly  the  case,  the  interval  between  the  first 
and  second  sound  may  be  prolonged,  and  as  this  marks 
the  duration  of  the  systole  it  shows  that  the  ventricle  is 
endeavouring  to  cope  with  the  difficulty  and  to  complete 
its  contraction.  The  short  or  systolic  pause  may  be  so 
prolonged  as  to  equal  the  diastolic  or  long  pause,  and  the 
sounds  thus  become  equidistant,  the  first  also  having 
become  short  and  sharp ;  the  only  difference  between  the 
sounds  is  one  of  emphasis  or  of  pitch,  and  it  is  often 
difficult  to  say  which  is  which.  The  sounds  may  be 
compared,  when  the  heart  is  acting  slowly,  to  the  ticking 
of  a  clock ;  when  rapidly,  to  the  puffing  of  a  distant 
locomotive. 

On  the  other  hand,  the  first  and  second  sounds  may  be 
approximated,  and  as  we  cannot  suppose  that  a  dilated  and 
enfeebled  ventricle  completes  its  systole  in  a  shorter  time 
than  normal,  the  only  possible  explanation  is,  that  it   is 


DILATATION.  297 

quickly  brought  up  short  by  the  resistance  in  the  arterial 
system  and  expels  but  a  small  proportion  of  its  contents. 
This  abbreviation  of  the  systolic  pause  is  therefore  a  serious 
indication  of  failure  of  the  ventricles,  and  when  carried  to 
an  extreme,  so  that  the  second  sound  follows  the  first 
immediately  and  almost  seems  to  overtake  it,  is  significant 
of  immediate  danger. 

In  two  successive  attacks  of  symptoms  due  to  dilatation 
of  the  heart,  when  the  degree  of  dilatation  appears  to  be 
exactly  the  same,  a  difference  in  the  length  of  the  systolic 
interval  is  sometimes  the  chief,  if  not  the  only,  point 
which  makes  a  difference  in  the  prognosis.  The  first  and 
second  sounds  are  spaced  in  the  first  attack,  which  is  sur- 
vived, and  approximated  in  the  second,  which  proves  fatal. 

Symptoms. 

The  symptoms  which  attend  the  earlier  stages  of 
dilatation  are  extremely  varied  and  often  very  vague.  An 
imperfect  and  fluctuating  supply  of  blood  to  the  brain  will 
give  rise  to  impairment  of  bodily  and  mental  energy,  and 
to  irresolution  and  vacillation  of  purpose ;  the  memory  is 
liable  to  fail,  especially  in  regard  to  recent  events,  and 
the  power  of  sustained  attention  and  consecutive  thought 
is  diminished.  The  frame  of  mind  will  often  be  despondent, 
and  the  temper  may  be  irritable.  There  may  be  attacks  of 
giddiness  or  faintness.  Sleep  is  usually  disturbed,  and  some- 
times almost  absent,  and,  whether  the  nights  are  good  or  bad, 
there  may  be  slumber  at  any  period  of  the  day,  the  patient 
dropping  off  to  sleep  even  over  his  morning  newspaper. 
For  the  same  reason,  viz.  the  irregular  and  imperfect  blood 
supply  and  the  back  pressure  in  the  veins,  digestion  and 
the  action  of  the  liver  will  be  deranged.  The  appetite 
is  bad,  and  food  is  followed  by  discomfort  and  by  flatulent 
distension,  which  latter  again  reacts  on  the  heart,  and  gives 


298  HEART  DISEASE. 

rise  to  oppression,  or  palpitation,  or  irregular  action.  The 
bowels  are  usually  torpid.  The  urine  is  deficient  in  amount 
and  high  coloured,  and  there  is  often  an  habitual  deposit 
of  urates.  Turbidity  of  the  urine  day  after  day,  whatever 
the  food  and  drink,  or  weather,  or  mode  of  life,  should 
direct  attention  to  the  state  of  the  circulation. 

There  is  no  one,  and  scarcely  any  combination,  of  the 
symptoms  enumerated,  however,  which  may  not  occur 
independently  of  weakness  and  dilatation  of  the  heart, 
especially  in  states  of  system  attended  with  high  tension ; 
and  it  would  be  waste  of  time  to  attempt  to  disentangle 
those  directly  due  to  the  state  of  the  heart  from  those 
which  are  merely  accidentally  associated  with  it. 

The  special  symptom  which  calls  attention  to  the  heart 
as  the  probable  starting-point  of  a  number  of  ailments  is 
breathlessness  on  slight   exertion,  but   even  this  may  be 
produced  by  other  causes — by  anaemia,  for  example ;  after 
middle   age,   pernicious    ansemia   may   often   give   rise   to 
extreme  breathlessness,  which  may  excite  a  suspicion  of 
heart  disease.     High  arterial  tension  alone,  which  has  not 
yet  given  rise  to  dilatation,  simple  debility,  sedentary  habits, 
with  a  tendency  to  corpulence,  may  also  cause  shortness  of 
breath.    These  facts  are  mentioned  in  order  to  warn  against  a 
too  ready  inference  that  dilatation  of  the  heart  exists  simply 
because  the  breath  is  short.     An  interesting  fact  in  connec- 
tion with  breathlessness  due  to  dilatation  of  the  heart  is 
that  it  is  often  relieved  by  exercise  of  the  voice.     I  have 
met    with   several   instances    in   which    a    clergyman   has 
climbed  into  the  pulpit  with  the  utmost  difficulty,  and  has 
not  only   preached   a  sermon  comfortably,   but   has   been 
all  the  better  for  it.     A  sense  of  breathlessness  coming  on 
during  repose,  and  inciting  the  patient  to  make  frequent 
deep  inspirations,  is  usually  a  symptom  of  nervous  depres- 
sion, and  has  no  necessary  relation  to  heart  disease.     Eor 
the  most  part,  as  the    disease   advances,   symptoms   arise 


DILATATION.  299 

which  are  indicative  of  back  pressure  in  the  systemic 
veins,  a  gradually  advancing  cedema  of  the  legs,  congestion 
of  the  lungs,  etc. 

In  an  extreme  case  the  patient  will  be  dropsical,  oedema 
invading  the  thighs,  loins,  and  abdominal  parietes,  as  well 
as  the  legs,  and  there  may  be  fluid  in  the  abdomen,  and 
perhaps  in  one  or  both  pleural  cavities.  The  feet  and  legs 
will  be  cold  and  pale,  or  purple  and  livid,  especially  if  hang- 
ing down  ;  the  hands  also  will  be  cold,  and  are  often  crimson 
or  purplish,  and  the  nails  of  a  deep  or  dusky  tint,  instead  of 
a  bright  pink.  A  white  patch  on  the  hand,  produced  by 
pressure,  is  very  slowly  invaded  by  returning  colour.  The 
sufferer  is  probably  unable  to  lie  down  in  bed,  and  is 
propped  up  by  pillows,  or  he  must  have  his  legs  down, 
and  therefore  spends  day  and  night  seated  in  his  chair. 
Remarkable  exceptions,  however,  are  met  with  in  this 
respect,  some  sufferers,  while  extremely  ill,  being  able  to 
lie  down  without  distress.  The  face  is  pale,  and  perhaps 
puffy,  especially  under  the  eyes,  with  injected  capillaries 
over  the  cheeks,  and  wears  an  expression  of  distress,  and 
the  eyes  are  watery.  The  lips  are  pale  or  bluish ;  the 
breathing  is  more  or  less  laboured,  even  in  repose,  and 
the  sufferer  constantly  supplements  his  reflex  respiration 
by  voluntary  deep  breaths.  When  he  speaks  it  is  in 
fragmentary  sentences,  and  with  evident  effort  and  aggrava- 
tion of  the  respiratory  distress.  The  least  movement  brings 
on  shortness  of  breath,  which  is  often  painful,  even  to 
witness.  The  pulse  is  frequent,  irregular,  and  probably 
greatly  deficient  in  tension.  The  urine  will  be  scanty,  of 
a  deep  colour,  and  high  specific  gravity ;  it  most  commonly 
throws  down  a  copious  deposit  of  brickdust  lithates,  and  it 
may  contain  albumen,  the  amount  of  which  may  vary  from 
day  to  day.  The  appetite  will  be  bad,  and  there  may  be 
nausea ;  the  tongue  may  be  furred,  the  bowels  constipated 
or   irregular.     One    of  the   most  distressing  symptoms    is 


300  HEART  DISEASE. 

sleeplessness,  and  when,  after  hours  of  Aveary  shifting  of 
position,  the  sufferer  is  overcome  by  fatigue  and  drops  off, 
he  has  painful  dreams,  and  wakes  suddenly  in  affright  and 
suffocation  for  lack  of  voluntary  help  to  his  respiration. 
The  longest  and  best  sleep  will  be  obtained  while  sitting 
in  a  chair,  and  sometimes  by  day  rather  than  in  the  night. 

The  jugulars  will  be  found  full,  but  not,  as  a  rule,  greatly 
distended  or  pulsating  forcibly.  The  liver  will  be  enlarged, 
coming  down  sometimes  as  low  as  the  umbilicus,  and  extend- 
ing across  the  epigastrium  into  the  left  hypochondrium.  It 
will  often  be  jogged  by  the  right  ventricle,  but  does  not 
usually  exhibit  true  expansile  pulsation.  The  jugular  dis- 
tension and  pulsation,  as  was  pointed  out  by  Mackenzie  of 
Burnley,  may  be  greatly  exaggerated  by  pressure  on  the 
enlarged  liver.  There  may  be  fluid  in  the  peritoneal  or 
pleural  cavities,  more  commonly  not,  and  there  will,  in  most 
cases,  be  physical  signs  of  cedema  and  congestion  of  the 
lungs ;  occasionally  the  percussion  note  may  be  good  and 
the  entry  of  air  free  and  unattended  with  adventitious 
sounds  of  any  kind  to  the  very  base  of  both  lungs. 

Peognosis. 

We  may  consider  first  the  most  serious  case  where  the 
symptoms  present  are  such  as  have  just  been  described.  We 
are  called  upon  to  answer  the  question,  Has  the  patient  a 
chance  of  recovering  from  the  condition  described,  or  will 
he  die  ? 

The  first  element  in  the  judgment  to  be  formed  will  be 
the  urgency  of  the  symptoms,  and  special  importance  will 
attach  to  two  of  the  series — the  nausea  and  loss  of  appetite 
and  the  sleeplessness — from  the  effects  which  they  have 
on  the  patient's  strength.  Frecpient  vomiting  of  food  is  of 
very  grave  import,  not  only  because  the  patient  does  not 
get  the  benefit  of  the  nourishment,  but  because  it  shows 


DILATATION.  301 

that  the  stasis  in  the  abdominal  circulation  has  reached  a 
point  which  interferes  seriously  with  the  digestive  secre- 
tions. Attacks  of  faintness  and  of  extreme  exhaustion,  or 
of  severe  dyspnoea,  are  also  of  serious  import. 

It  is  not  always  when  the  dropsy  is  excessive  that  the 
condition  of  the  patient  is  worst.  From  the  late  appearance 
or  entire  absence  of  dropsy  in  fatty  degeneration  of  the  heart, 
in  aortic  disease,  and  mitral  stenosis,  it  would  appear  that  a 
certain  degree  of  pressure  in  the  arterial  system  is  required 
to  co-operate  with  the  back  pressure  in  the  venous  system 
for  the  full  development  of  dropsical  effusion;  and  when 
the  osdema  remains  moderate  in  amount,  while  other 
symptoms — such  as  breathlessness,  faintness,  and  muscular 
weakness,  the  latter  especially — indicate  great  cardiac 
inefficiency,  it  may  be  because  the  left  ventricle  propels 
the  blood  with  very  little  force.  Degeneration  may  be  a 
factor  in  the  case.  A  frequent,  short,  unsustained  pulse 
and  heart-beat,  without  much  oedema,  may  thus  indicate 
a  more  grave  condition  than  extreme  dropsy.  Long- 
continued  excessive  frequency  of  the  pulse  is  an  un- 
favourable sign. 

The  urgency  of  the  symptoms  being  about  the  same,  a 
greater  degree  of  dilatation,  as  indicated  by  a  more  extended 
area  of  dulness,  by  marked  displacement  of  and  diffuseness 
and  weakness  of  the  apex  beat,  will  add  gravity  to  the  prog- 
nosis. A  further  unfavourable  indication  will  be  approxima- 
tion of  the  first  and  second  sounds. 

When  the  symptoms  and  physical  signs  have  been  well 
weighed,  the  first  question  to  be  asked  in  view  of  prognosis 
is  whether  there  has  been  any  adequate  exciting  cause  of 
the  symptoms.  If  there  has  been  recognizable  over-exertion 
or  excitement,  or  grave  anxiety- — any  mental  or  bodily 
strain — or  if  there  has  been  a  chill,  giving  rise  to  bronchitis 
or  other  affection  of  the  lungs,  or  deranging  seriously  the 
liver  and  digestive  organs,  it  may  be  hoped  by  means  of 


302  HEART  DISEASE. 

rest  and  treatment  to  undo  the  ill-effects  and  restore  the 
balance.  If,  on  the  other  hand,  the  symptoms  have  crept 
on  gradually  without  traceable  cause  of  the  kind  mentioned, 
and  especially  when  due  care  has  been  exercised,  and  there 
has  been  no  habitual  error  of  regimen  or  neglect  of  bowels, 
the  probabilities  are  that  the  symptoms  are  the  outcome  of 
conditions  which  cannot  be  reversed — of  radical  inherent 
weakness  of  the  heart. 

The  previous  mode  of  life,  active  or  sedentary,  careful 
or  imprudent,  and  especially  the  habits  with  regard  to 
alcoholic  stimulants,  will  have  a  very  important  bearing  on 
the  probable  issue  of  the  attack,  as  will  also  the  general 
soundness  and  the  absence  or  existence  of  disease  of  any 
other  important  organs,  especially  of  the  kidneys  and  liver. 
The  patient's  cheerfulness,  hopefulness,  and  courage  under 
his  sufferings,  or  his  despondency,  will  make  powerfully  for 
or  against  him,  not  only  as  direct  influences,  but  because  the 
state  of  mind  is  often  an  index  of  the  state  of  the  system. 

Another  inquiry  of  great  prognostic  weight  will  be  as 
to  the  patient's  family  history.  It  is  through  this  that  we 
obtain  an  idea  of  his  vital  tenacity,  of  the  trustworthiness 
of  his  tissues,  and  of  the  special  liabilities  to  cardio-vascular 
degeneration.  There  are  few  tendencies  which  run  more 
strongly  in  families  than  those  which  are  manifested  in 
the  heart  and  vascular  system,  whether  to  high  arterial 
tension  with  the  effects  on  the  vessels  and  heart,  which 
follow  from  this,  or  to  dilatation  and  weakness,  or  to 
degeneration,  and  a  prognosis,  otherwise  not  unfavourable, 
might  have  to  be  instantly  revised  on  learning  that  the 
father,  an  uncle,  or  a  brother,  had  died  at  about  the  patient's 
age  from  heart  disease.  Finally,  the  response  to  treatment 
will  speedily  afford  an  indication  of  the  utmost  value. 


dilatation.  303 

Treatment. 

Mild  Cases. — In  view  of  the  tendency  to  dilatation  in 
acute    rheumatism   and    influenza,    and    after    any    acute 
bacterial  infection  when  the  heart  muscle  has  been  more 
or  less  damaged  by  toxins,  a  period  of  rest,  with  avoidance 
of  any  undue  exertion,  is  advisable  after  any  acute  illness. 
Loss  of  tone  of  the  cardiac  muscle,  with  a  certain  degree  of 
dilatation  of,  and,  it  may  be,  irritability  of,  the  heart,  is 
especially  liable  to  occur  after  an  attack  of  influenza,  and 
is  frequently  associated  with   mental  depression  and   loss 
of  nerve  tone.    This  class  of  case  is  usually  much  benefited 
by  the  "  Schott "  treatment  of  baths,  as  the  daily  routine, 
enforced  period  of  rest,  the  sedative  effect  of  the  baths,  the 
change  of  air  and  scene,  with  absence  of  excitement  and 
mental  exertion,  is  highly  beneficial.     It  is  by  no  means 
essential  that  the   patient  should  go  to  Nauheim,  as  the. 
treatment  can  be  carried  out  at  his  own  home  or  at  various 
bathing  stations  in  England,  e.g.  Bath,  Buxton,  Harrogate, 
and  other  places,  or,  if  the  patient  wishes  to  go  abroad,  at 
numerous  other  health  resorts ;  in  France,  for  instance,  as 
pointed  out  by  Huchard,  at  Chatel  Guyon,  Salins  Moutiers, 
Koyat,  etc.,  and  at  various  places  in  Germany.     This  hydro- 
therapeutic  treatment  is   usually  only  necessary  in  cases 
in  which  there  is  an  element  of  neurosis,  cardiac  irritability, 
or  mental  depression,  Avhen  the  psychological  element  must 
be  taken  into  consideration. 

In  slight  cases  of  dilatation  and  loss  of  tone,  a  complete 
holiday  from  work,  with  change  of  air  to  a  bracing  climate, 
will  usually  suffice.  Mild  cardiac  tonics  may  be  given, 
and  gentle  exercise  taken,  the  duration  of  which  should 
be  gradually  increased  day  by  day.  At  first,  rest  in  the 
recumbent  position  for  at  least  half  an  hour  before  meals 
should  be  insisted  on. 

Severe  Cases, — In  the  treatment  of  advanced  symptoms 


304  HEART  DISEASE. 

due  to  dilatation  of  the  heart,  we  have  to  deal  at  the  same 
time  with  defective  propulsive  power  on  the  part  of  the 
ventricle,  and  damming  back  of  blood  in  the  venous  system 
— the  former  being  the  primary  and  principal  difficulty — 
and  the  indications  are  to  relieve  the  ventricles  of  work  and 
give  them  strength,  and  at  the  same  time  to  deplete  the 
venous  engorgement. 

This  last  object  must,  indeed,  be  taken  first. 

Venesection,  the  most  effectual  means  of  relieving  the 
right  side  of  the  heart,  is  rarely  applicable  in  acute  dilata- 
tion. It  is  conceivable  that  under  some  pulmonary  com- 
plications resulting  from  chill,  the  engorgement  of  the 
right  ventricle  and  auricle  might  be  such  as  to  make  blood- 
letting the  less  of  two  dangers ;  but,  the  initial  fault  being 
weakness  of  one  or  both  ventricles,  we  cannot  trust  the 
heart  to  adjust  itself  to  a  rapid  change  of  any  kind,  and 
the  right  ventricle  may  not  be  in  a  condition  to  take 
advantage  of  the  relief  afforded  it.  Usually,  however,  the 
venous  engorgement  is  developed  slowly,  and  the  indica- 
tions for  venesection  do  not  arise. 

The  application  of  six  or  eight  leeches  over  the  liver  is 
safer,  and  it  will  usually  effect  all  that  can  be  done  by 
direct  abstraction  of  blood.  The  indication  for  this  local 
bleeding  is  enlargement  of  the  liver,  and,  when  this  is 
considerable,  it  rarely  fails  to  afford  striking  relief.  Fre- 
quently, for  example,  the  patient,  who  has  previously 
been  tortured  by  sleeplessness,  will  sleep  at  once  aud  some- 
times for  a  night  or  two  afterwards.  The  reason  for  selecting 
the  hepatic  region  for  the  application  of  the  leeches  is 
simply  that  pain  and  tenderness  felt  there  are  relieved; 
it  is  not  supposed  that  blood  is  drawn  from  the  liver,  or 
that  the  same  amount  abstracted  elsewhere  would  not  be 
equally  efficacious.  The  leeches  should  be  followed  by  a 
hot  fomentation,  which,  besides  encouraging  the  bleeding, 
will  bring  blood  to  the  surface.     When  the   liver  is  not 


DILATATION.  305 

enlarged,  and  especially  if  the  right  ventricle  impulse  and 
sounds  are  weak,  there  is  no  advantage  to  be  gained  by- 
leeching. 

Concurrently  with  the  application  of  leeches  a  purgative 
will  be  given,  which  will  deplete  the  portal  system  at  the 
same  time  that  the  leeching  depletes  the  systemic  veins. 
Afterwards  this  will  be  the  principal  means  of  keeping  down 
the  venous  engorgement.  In  a  large  majority  of  cases, 
indeed,  we  have  to  depend  entirely  upon  purgatives  for  this 
purpose,  as  abstraction  of  blood  by  any  method  is  inadmis- 
sible. It  is  not  a  matter  of  indifference  what  purgatives  are 
employed.  The  object  of  a  purgative  is  not  simply  to  carry 
off  as  much  fluid  as  possible  and  so  drain  the  tissues.  This 
may  be  the  case,  perhaps,  in  ascites  from  cirrhosis  of  the 
liver ;  but  in  heart  disease  of  any  kind,  and  especially  in 
dilatation,  much  more  is  to  be  gained  by  rectifying  the 
balance  of  the  circulation :  the  kidneys  will  then  often 
resume  their  function  and  remove  the  excess  of  liquid. 

Purgatives,  then,  may  be  made  to  contribute  to  this ;  and 
before  considering  them  further  we  must  refer  to  the  first 
object  of  treatment,  the  relief  of  the  heart  from  work  and 
the  increase  of  its  vigour.  Of  these  we  can  be  much  more 
sure  of  the  first  than  of  the  second ;  we  can  more  easily  and 
certainly  diminish  the  resistance  in  the  arterioles  and 
capillaries  than  we  can  lend  strength  and  efficiency  to  the 
action  of  the  heart,  and,  without  removing  the  obstruction 
in  the  peripheral  circulation,  it  might  only  do  harm  to 
incite  the  heart — weakened  as  its  structures  are — to  greater 
effort  to  overcome  it.  Mercurial  purgatives  have  this  effect 
of  diminishing  arterio-capillary  resistance  and  of  lowering 
arterial  tension,  and  therefore  of  relieving  the  heart.  This 
is  a  fact  of  clinical  experience  and  observation,  and  its 
explanation  is  a  matter  of  secondary  importance,  but  the 
hypothesis  by  which,  as  it  seems  to  me,  it  is  best  explained, 
is  that  mercury  influences  the  liver  metabolism  and  promotes 

x 


306  HEART  DISEASE. 

the  elimination  of  impurities  which,  when  retained  in  the 
blood,  give  rise  to  resistance  in  the  capillaries.  But, 
whatever  the  explanation,  the  fact  that  the  arterial  tension 
is  notably  lowered  by  mercurial  aperients  is  one  which  is 
confirmed  by  daily  experience.  It  is  remarkable  how 
frequently  the  statement  recurs  in  works  on  heart  disease 
that  other  remedies  often  fail  to  act  until  a  dose  of  calomel 
or  other  mercurial  preparation  has  been  given. 

Mercurial  purgatives,  then,  have  the  double  effect  of 
depleting  the  portal  system,  which  relieves  the  enlargement 
of  the  liver  and  the  distension  of  the  right  side  of.  the  heart, 
and  of  diminishing  the  resistance  in  the  peripheral  circula- 
tion, and  so  relieving  the  left  ventricle  of  stress.  Very 
commonly  the  best  of  testimony  as  to  the  beneficial  character 
of  the  result  is  given  by  refreshing  sleep.  The  disadvantage, 
if  such  it  be,  that  less  fluid  is  carried  off  than  by  hydragogue 
cathartics  is  often  compensated  by  an  increased  flow  of 
urine ;  and  elaterium,  gamboge,  pulv.  jalap,  co.,  and  the  like, 
when  repeated,  give  rise  to  great  exhaustion. 

Calomel,  then,  or  blue  pill  or  grey  powder,  should  be 
given  in  doses  of  from  1  to  5  grains,  according  to  the 
urgency  of  the  case,  with  colocynth  and  hyoscyamus  or 
rhubarb,  followed  by  some  mild  saline.  After  one  or  more 
full  doses  at  the  outset,  a  moderate  dose  may  be  given 
every  third  or  fourth  night.  The  acid  tartrate  of  potash 
will  often  co-operate  beneficially,  both  by  its  action  on  the 
bowels  and  on  the  kidneys. 

The  heart  being  relieved  of  work  may  be  urged  to  more 
vigorous  contraction  by  digitalis,  strophanthus,  spartein, 
squills,  caffein,  convallaria,  apocyanum,  the  special  heart 
tonics,  with  which  strychnine  may  usually  be  combined  with 
advantage.  In  a  case  of  extreme  suffering,  digitalis  may 
be  given  with  ammonia,  ether,  and  nux  vomica ;  in  a  more 
chronic  stage,  with  iron,  strychnine,  and  perhaps  nitric  or 
hydrochloric  acid.      Sometimes   an  effect  can  be  obtained 


DILATATION.  3"7 

by  giving  diuretin  or  caffein  in  a  cachet,  at  the  same  time 
with  digitalis  in  a  mixture,  when  singly  neither  seems  to 
be  efficacious.  Squills,  again,  may  be  given  with  digitalis 
as  in  the  well-known  pill  with  mercury,  or  in  some  liquid 
combination.  Next  to  digitalis  stands  strophanthus,  which 
is  a  most  valuable  alternative  when  digitalis  seems  to 
produce  sickness,  as  is  sometimes  the  case,  or  when  it  fails 
to  exercise  a  favourable  influence  on  the  heart.  Sulphate 
of  spartein  I  have  seen  to  be  of  great  service  when  digitalis 
and  strophanthus  appeared  to  have  exhausted  their  influence. 
Of  convallaria  I  have  little  to  say.  Apocyanum  has,  in  one 
or  two  cases,  seemed  to  carry  off  dropsy  in  a  remarkable 
way,  but  one  patient  died  suddenly  when  apparently  just 
well. 

It  is  not  necessary  to  go  into  greater  detail  with  regard 
to  these  remedies.  Throughout  a  case  of  the  kind  the 
medical  man  has  to  fight,  so  to  speak,  with  both  hands,  and 
continuous  watchfulness  will  be  necessary  to  meet  the 
vicissitudes  which  occur,  and  many  changes  in  method 
may  be  required,  while  the  same  principles  are  held  in 
view. 

The  prognosis,  as  has  been  said,  will  be  greatly  influenced 
by  the  response  to  treatment.  This  will  be  energetic, 
especially  in  the  matter  of  purgatives,  in  proportion  as  the 
symptoms  are  urgent,  and  if  no  favourable  effect  is  produced, 
the  prospect  of  recovery  is  very  poor.  Very  commonly 
improvement  takes  place  up  to  a  certain  point,  and  then 
progress  seems  to  come  to  an  end.  This  is  a  trying  stage 
both  to  the  patient  and  to  the  medical  man.  Change  of 
remedies  and  new  combinations  must  be  tried,  both  in 
regard  of  the  aperient  and  of  the  tonic,  not  frequently  and 
capriciously,  but  with  careful  study  of  the  results  and  due 
allowance  of  time  for  obtaining  them.  Sometimes  it  does 
good  to  suspend  all  medicines  for  a  few  days  and  start 
afresh.    When  the  oedema  of  the  legs  is  considerable,  it  may 


3oS  HEART  DISEASE. 

be  of  the  greatest  service  to  drain  the  fluid  from  the  legs. 
The  good  result  of  removing  an  ascitic  accumulation, 
should  this  be  present,  may  be  still  more  striking.  Even 
a  moderate  amount  of  effusion  in  the  pleural  cavity,  such 
as  we  should  not  think  of  dealing  with  under  ordinary 
circumstances,  should  be  aspirated.  A  straw  may  turn  the 
balance  either  way,  and  a  very  slight  obstacle  may  prevent 
the  heart  from  regaining  control  over  the  circulation.  It 
is  not  always  desirable  to  postpone  the  removal  of  fluid  till 
the  particular  conjuncture  described  arrives ;  it  may  be  an 
urgent  necessity  at  a  very  early  period.  Usually,  however, 
it  is  prudent  to  give  remedies  a  chance  before  resorting  to 
puncture  or  paracentesis.  As  regards  the  method  of  drainage 
to  be  employed,  Southey's  tubes  are,  in  my  opinion,  much 
the  best,  whether  for  oedema  or  ascites,  but  particularly 
in  case  of  ascites,  as  the  too  rapid  removal  of  the  fluid 
is  inadvisable. 

Dropsy. — It  has  been  found  that  in  Bright's  disease  with 
oadema  and  ascites  the  dropsical  fluids  are  rich  in  chlorides. 
Normally,  the  proportion  of  chlorides  in  the  blood  and 
urine  is  a  stable  quantity,  and  any  excess  of  chlorides 
ingested  is  eliminated  in  the  urine.  In  Bright's  disease 
there  is  usually  deficient  elimination  of  salts  in  the  urine 
and  an  excess  in  the  blood.  It  is  argued,  therefore,  that 
when  the  kidneys  are  diseased,  and  there  is  defective 
elimination  of  salts,  the  accumulation  of  salts,  more 
especially  chlorides  in  the  blood,  favours  the  production 
of  dropsy.  Widal,  indeed,  claims  that  he  can  in  certain 
cases  of  Bright's  disease  provoke  or  abolish  dropsy  at  will, 
simply  by  the  administration  or  withholding  of  sodium 
chloride  in  the  diet.  Though  this  is  not  altogether  proved 
in  the  case  of  cardiac  dropsy,  it  is  advisable,  in  view  of  these 
observations,  to  eliminate  from  the  diet  common  salt  and 
other  chlorides,  as  far  as  possible. 

The  feeding  of  the  patient  through  the  long  course  of 


DILATATION.  309 

treatment  will  be  a  task  of  extreme  difficulty.  We  have 
to  contend  with  nausea  and  distaste  for  food  amounting  to 
disgust ;  sometimes  the  sufferer  positively  cannot  swallow 
anything  requiring  mastication.  The  object  to  be  held 
in  view  is  to  keep  down  the  volume  of  the  blood  while 
maintaining  its  quality.  A  small  amount  of  solid  or  semi- 
solid food  should  be  taken  about  every  three  hours.  When 
the  patient  is  not  too  ill  to  take  his  meals  at  the  accustomed 
times  it  is  a  great  encouragement  to  him  to  be  allowed  to 
do  so,  and  he  may  then  eat  what  he  can  of  fish,  fowl,  tender 
meat,  and  milk  puddings.  When  the  appetite  is  small 
the  regular  meals  may  be  supplemented  by  intermediate 
nourishment,  such  as  a  beaten-up  egg,  a  little  milk,  or 
perhaps  a  small  cup  of  beef-tea,  or  a  little  beef  or  chicken 
jelly,  or  meat  extract.  Soups  and  jellies  have  the  dis- 
advantage of  containing  little  proteid  and  much  liquid, 
and  many  extractives  and  salts,  but  they  are  stimulants 
to  the  flagging  heart.  Potted  meat  sandwiches  are  a  great 
resource,  and  the  pulp  of  raw  beefsteak  can  be  given  in  this 
form,  disguised  by  cooked  meat  or  concentrated  gravy.  A 
German  method  of  treatment  is  to  feed  patients  suffering 
from  cardiac  dropsy  entirely  on  raw  ham. 

The  amount  of  fluid  must  be  restricted  as  far  as  possible, 
especially  that  taken  with  food.  Stimulants  are  usually 
necessary,  but  should  be  kept  within  limits  known  to 
and  defined  by  the  medical  man.  The  patient  is  under 
a  great  temptation  to  resort  to  them  for  the  relief  of 
faintness,  exhaustion,  and  nausea.  Cream  of  tartar  drink 
may  be  taken  to  quench  thirst  between  meals,  and  in  some 
cases  a  copious  draught  of  hot  water  once  or  twice  a  day 
will  run  through  the  system  rapidly  and  wash  out  the 
organs  and  tissues  without  augmenting  permanently  the 
volume  of  the  blood  or  adding  to  the  dropsy.  When  this 
is  tried  it  must  be  ascertained  definitely  that  the  amount 
of  urine  is  correspondingly  increased. 


3io  HEART  DISEASE. 

A  question  which  arises  in  almost  every  severe  case  is 
whether  the  patient  must  be  urged  to  remain  in  bed  or 
allowed  to  get  up.  Bed  is  undoubtedly  the  best  place  for 
him  at  first,  during  what  may  be  called  the  crisis  of  the 
attack,  for  many  reasons ;  the  rest  and  warmth  protect  the 
heart  from  the  strain  of  exertion  and  changes  of  temperature. 
On  the  other  hand,  the  dyspnoea  is  usually  worse  in  the 
recumbent  posture,  even  with  the  shoulders  raised,  and  may 
be  intolerable  unless  the  legs  are  allowed  to  hang  down ; 
not  unfrequently  it  is  simply  impossible  for  the  patient  to 
remain  in  bed.  A  suitable  chair,  therefore,  is  necessary, 
with  support  for  the  elbows,  shoulders,  and  head,  which 
can  be  taken  advantage  of  in  turn  in  the  frequent 
changes  of  position  to  which  the  patient  has  recourse  to 
ease  his  breathing  or  elude  discomfort,  and  the  quickness 
and  ingenuity  of  the  medical  man  or  nurse  in  devising 
expedients  may  greatly  alleviate  his  sufferings.  A  bed 
table  or  other  form  of  support,  upon  which  the  patient  may 
rest  his  arms  or  elbows  and  head  when  leaning  forwards 
while  sitting  in  his  chair,  will  often  be  useful.  A  patient 
will  frequently  sleep  better  in  this  position  than  in  any 
other.  Perhaps  the  most  common  state  of  things  is  that 
the  patient  is  up  during  the  day,  and  tries  to  spend  more 
or  less  of  the  night  in  bed.  When  he  cannot  at  once 
bear  to  go  to  bed  at  night,  he  may  undress  and  sit  in  his 
chair  wrapped  in  blankets  near  the  bed,  when  he  will 
often,  after  a  time,  be  able  to  lie  down  and  sleep. 

Small  doses  of  morphia  may  be  given  hypodermically 
to  enable  the  patient  to  get  a  little  sleep  and  relief  from 
his  sufferings.  Little  benefit  can  be  expected  at  this  stage 
from  the  administration  of  cardiac  tonics  which  will  have 
been  freely  given  at  an  earlier  period.  The  heart  is  past 
recovery,  and  all  that  can  be  done  is  to  treat  symptoms 
as  they  arise  and  give  temporary  relief  as  far  as  is  possible. 


CHAPTER  XXI. 

STRUCTURAL   CHANGE   IN   THE   RIGHT 
VENTRICLE. 

PHYSIOLOGICAL     DILATATION — HYPERTROPHY    AND    DILATA- 
TION— DEGENERATION    OF    THE    MUSCULAR    WALLS. 

Dilatation  and  hypertrophy  of  the  right  ventricle  are 
perhaps  the  most  common  of  all  the  structural  changes 
to  which  the  heart  is  subject.  Some  primary  dilatation 
accompanies  all  severe  exertion,  and  when  the  exertion 
has  been  inordinate  it  may  be  considerable  and  persist  for 
some  time,  but  unless  the  muscular  fibres  have  undergone 
degeneration  from  age  or  abuse  of  alcohol,  or  a  sedentary 
life,  or  from  recent  febrile  disease,  or  diphtheria,  there  is  a 
wonderful  power  of  recovery.  If  over-exertion  is  habitual 
the  dilatation  will  be  neutralized  by  hypertrophy.  In  all 
cases  of  valvular  disease  of  the  left  ventricle  or  of  lung 
disease,  such  as  bronchitis,  emphysema,  etc.,  which  give 
rise  to  obstruction  in  the  pulmonary  circulation,  dilatation 
and  hypertrophy  of  the  right  ventricle  follow  as  a  necessary 
physiological  result,  as  has  already  been  explained  in  a 
previous  chapter. 

Dilatation  and  hypertrophy  of  the  right  ventricle  are 
thus,  for  the  most  part,  pathological  in  name  only,  and  are 
really  compensatory  adjustments  which  neutralize  more  or 
less  perfectly  the  effects  of  valvular  or  other  disease  of  the 
left  side  of  the  heart,  and  when  compensation  is  effectual 
become  an  indication  of  the  degree  of  severity  of  the 
original  disease. 


312  heart  disease. 

Physical  Signs  and  Symptoms. 

Hypertrophy  or  Dilatation  of  the  right  ventricle  carries 
the  apex  of  the  heart  to  the  left  and  increases  the  hori- 
zontal dimensions  of  the  heart.  The  apex  beat  may  be 
found  at  or  beyond  the  vertical  nipple  line,  not  unfre- 
quently  in  the  anterior  or  even  mid-axillary  line,  when 
there  is  also  enlargement  of  the  left  ventricle.  The  cha- 
racter of  the  apex  beat  depends  more  on  the  left  ventricle 
than  the  right,  but  with  much  dilatation  of  the  right 
ventricle  it  is  usually  diffuse.  The  area  of  cardiac  dulness 
will  be  increased,  and,  on  percussion,  it  may  be  found  that 
the  area  of  dulness  extends  to  the  right  or  considerably 
beyond  the  right  margin  of  the  sternum  and  upwards  to 
the  second  rib,  in  consequence  of  the  dilatation  of  the 
right  auricle,  which  usually  coexists  with  the  dilatation 
of  the  ventricle,  which  is  evident  from  its  pulsation  in  the 
epigastrium. 

The  degree  of  hypertrophy  is  estimated  by  the  force  of 
the  right  ventricle  impulse  as  communicated  to  the  hand 
applied  over  the  lower  left  costal  cartilages  and  the 
epigastrium,  and  also  by  the  degree  of  accentuation  of  the 
pulmonic  second  sound.  It  is  the  degree  of  hypertrophy 
which  is  of  vital  importance,  as  on  this  depends  the 
efficiency  of  compensation. 

The  symptoms  usually  associated  with  the  changes  in 
the  right  ventricle  just  described  are  pulmonary  congestion, 
venous  stasis,  and  dropsy,  but  these  are  not  so  much  the 
effects  of  dilatation  of  the  right  ventricle  as  the  final  results 
of  the  original  disease  of  the  left  ventricle  or  lungs,  which 
the  right  ventricle  has  been  unable  to  combat  efficiently. 

It  has  seemed  to  me  that  our  ideas  of  the  effects  of 
disease  of  the  right  ventricle  have  been  too  much  based 
upon  a  study  of  the  symptoms  which  attend  affections  of 
this  ventricle  secondary  to  disease  of  the  left  ventricle  or 


HYPERTROPHY  &  DILATATION  OF  RIGHT  VENTRICLE.      313 

its  valves,  which  therefore  are  really  attributable  to  the 
original  disease. 

Undoubtedly  the  supervention  of  dilatation  of  the  right 
ventricle  and  of  reflux  through  the  tricuspid  orifice  allows 
back  pressure  to  be  brought  to  bear  upon  the  veins,  but 
this  only  intensifies  pre-existing  effects  and  symptoms,  and 
makes  no  change  in  their  character. 

We  are  perhaps  justified  in  assuming  that  the  venous 
back  pressure,  to  which  insufficiency  of  the  tricuspid  valve 
will  give  rise,  will  in  some  degree  produce  the  same  results, 
whatever  the  state  of  the  left  side  of  the  heart,  and  whether 
or  not  the  tricuspid  regurgitation  has  been  caused  by 
obstruction  in  the  pulmonary  circulation;  but  the  condi- 
tions are  fundamentally  different  when  the  tricuspid  reflux 
is  primary.  It  is  not  impossible,  for  example,  that  a  sound 
and  strong  left  ventricle  may  come  to  the  aid  of  the  right 
ventricle,  just  as  the  right  ventricle  so  constantly  comes 
to  the  aid  of  the  left,  notwithstanding  the  great  length  of 
the  systemic  as  compared  with  the  pulmonic  circuit  and 
the  weak  blood  pressure  in  the  systemic  veins.  The  pressure 
which  will  cause  the  blood  to  spurt  for  two  or  three  feet 
in  venesection  might  carry  a  current  through  the  capillaries 
of  the  lungs  aided  by  the  respiratory  movements  and  the 
valves  of  the  pulmonary  artery. 

It  has,  moreover,  seemed  to  me  that  weakness  of  the 
right  ventricle — the  left  ventricle  being  in  a  normal  con- 
dition— has  in  some  cases  given  rise  to  symptoms  due 
rather  to  inadequate  supply  of  blood  to  the  left  side  of  the 
heart  than  to  damming  back  of  blood  in  the  veins.  I  have, 
for  example,  met  with  several  instances  of  primary  tricuspid 
regurgitation,  either  as  a  constant  condition  or  coming  on 
under  very  slight  provocation.  When  any  effect  of  this 
has  been  traceable  it  has  not  been  breathlessness  on 
exertion,  but  tendency  to  syncope.  Perhaps  this  is  what 
we   ought   to    expect,   since    the    occurrence    of   tricuspid 


314  HEART  DISEASE. 

regurgitation  in  the  breathlessness  of  violent  exertion  has 
been  regarded  as  a  safety-valve  action,  by  lowering  the 
pressure  in  the  pulmonic  circulation.  A  difference  of 
symptoms  ought  to  attend  mitral  and  tricuspid  insuffi- 
ciency, one  giving  rise  to  turgescence  and  high  pressure 
in  the  pulmonary  circulation,  the  other  to  deficient  supply 
of  blood  and  low  pressure.  If  mitral  disease  produces 
pulmonary  symptoms,  tricuspid  disease  may  well  produce 
systemic  symptoms. 

In  a  few  cases  which  have  come  under  my  notice,  in 
which  the  right  ventricle  has  appeared  to  be  predominantly 
or  almost  exclusively  affected  by  asthenia  or  degenera- 
tion, the  effects  have  been  similar  to  those  of  tricuspid 
regurgitation. 

A  master  in  a  public  school,  who  had  been  accustomed 
to  vigorous  exercise,  received  a  severe  blow  on  the  chest. 
He  had  for  some  time  great  pain  in  the  cardiac  region, 
and  when  he  walked  he  soon  felt  faint.  When  I  saw  him 
some  time  after  the  injury  he  had  had  slight  but  distinct 
syncopal  attacks.  On  examination,  no  valvular  disease 
was  present,  and  the  heart  was  of  normal  size.  There  was 
a  fair  apex  push  in  the  normal  situation,  and  the  left 
ventricle  first  sound  and  the  aortic  second  sound  were 
normal  in  character.  JSTo  right  ventricle  impulse,  how- 
ever, could  be  detected,  and  its  first  sound  and  the  pulmonic 
second  sound  were  very  weak. 

What  had  happened  exactly  cannot  be  stated,  but  from 
the  contrast  between  the  action  and  sounds  of  the  two  sides  of 
the  heart,  it  seemed  as  if  the  right  ventricle  had  been  in  some 
way  injured,  and  that  its  contractile  energy  was  impaired. 

The  patient  regained  the  power  of  taking  exercise,  and 
with  this  the  sounds  of  the  right  ventricle  became  normal. 

A  patient,  aged  72,  who  had  never  had  a  day's  illness 
in  his  life,  consulted  me  in  1879,  complaining  of  failing 
vigour,  giddiness  on  running  to  catch  a  'bus,  tendency  to 


HYPERTROPHY  &°  DILATATION  OF  RIGHT  VENTRICLE.      315 

fall  asleep  in  the  day.  He  was  constipated ;  the  pulse, 
which  was  not  more  than  60,  was  sometimes  tense,  some- 
times soft.  The  heart  sounds  generally  were  weak,  the 
aortic  second  accentuated.  In  April,  1881,  symptoms, 
which  had  previously  been  relieved,  returned,  and  it  was 
now  found  that  over  all  parts  of  the  right  ventricle,  and 
even  over  the  pulmonic  area,  there  was  absolute  silence. 
No  impulse  or  apex  beat  could  be  detected,  but  at  the  apex 
the  sounds  were  normal ;  the  aortic  second  sound  was 
accentuated.  The  pulse  was  72,  a  little  irregular,  but  fair 
in  force  and  length.  A  month  later  he  was  much  better. 
The  pulse  was  60,  fair  in  strength  and  length ;  the  left 
ventricle  sounds  were  good,  the  right  ventricle  sounds 
faintly  audible.  From  this  time  neither  the  right  ventricle 
first,  nor  the  pulmonic  second  sound  were  ever  at  any  time 
audible.  The  pulse  varied  considerably  both  in  frequency 
and  in  tension,  but  it  was  usually  well  sustained,  indicating 
considerable  vigour  of  the  left  ventricle,  and  the  left 
ventricle  sounds  were  good.  He  had  from  time  to  time 
severe  fainting  attacks,  which  sometimes  threatened  to 
prove  fatal.  He  was  always  worse  when  the  bowels  were 
not  kept  freely  open.  In  June,  1883,  the  pulse  is  described 
as  large,  full,  and  tense ;  the  aortic  second  sound  was 
accentuated  at  the  apex  and  in  the  right  second  space  ; 
there  were  no  right  ventricle  sounds  whatever.  Towards 
the  end  of  1884,  when  not  under  my  care,  the  bowels  were 
allowed  to  get  confined,  and  he  fell  into  a  condition  of 
torpor,  with  incontinence  of  urine  and  faeces.  He  recovered 
from  this  condition  after  free  purgation,  and  was  again  able 
to  go  about,  though  his  mental  faculties  were  impaired 
and  he  was  childish ;  but  in  November,  1885,  thrombosis 
of  the  left  middle  cerebral  artery  took  place,  giving  rise  to 
hemiplegia  and  aphasia,  of  which  he  died. 

The  entire  absence  of  right  ventricle  sounds   in   this 
case  was  very  remarkable,  and  I  cannot  doubt  that  there 


3l6  HEART  DISEASE. 

was  a  very  feeble  action  of  this  ventricle.  As  it  seemed  to  me 
impossible  that  the  pulmonary  circulation  could  be  main- 
tained without  its  aid,  I  formed  a  very  unfavourable 
prognosis ;  and  when  this  was  belied  I  watched  the  case 
with  extreme  care,  first  to  make  sure  that  my  observation 
was  not  at  fault,  and  next  in  order  that  I  might  arrive  at 
some  comprehension  of  the  problem  presented  by  the  facts. 
The  conclusion  appeared  to  be  unavoidable  that  the  left 
ventricle  was  carrying  on  the  circulation  through  the 
lungs;  it  was  throughout  capable  of  maintaining  high 
tension  in  the  arteries.  The  amount  of  blood  passing 
through  the  pulmonary  vessels  under  these  conditions  and 
reaching  the  left  auricle  would  be  easily  influenced,  and 
would  vary  greatly,  and  the  fluctuating  supply  of  blood  to 
the  left  ventricle  would  account  for  the  varying  character 
of  the  pulse. 

One  of  the  most  serious  effects  of  weakness  of  the  right 
ventricle  is  met  with  in  disease  of  the  mitral  valve.  When 
the  mitral  valve  is  incompetent,  or  from  thickening  and 
shrinking  of  the  curtains  and  tendinous  cords  becomes 
stenosed,  the  right  ventricle  is  for  a  time  the  rampart  by 
which  the  reflux  of  blood  is  arrested,  or  increased  pressure 
in  the  left  auricle  is  maintained  to  promote  a  more  rapid 
flow  through  the  narrowed  orifice.  When  we  hear  an  apex 
murmur  telling  of  mitral  regurgitation  or  stenosis,  the 
murmur  itself  gives  no  trustworthy  information  as  to  the 
severity  of  the  lesion.  We  gather  this  mainly  from  the 
effects  upon  the  right  ventricle.  The  first  of  these  is 
accentuation  of  the  pulmonic  second  sound,  indicating 
increased  pressure  in  the  pulmonary  circulation,  and  fol- 
lowing on  this  hypertrophy  of  the  right  ventricle,  by  means 
of  which  the  obstruction  to  the  passage  of  blood  through 
the  lungs  is  overcome.  It  is  by  the  augmented  strength 
of  the  right  ventricle  that  the  mitral  leakage  or  obstruction 
is  neutralized  and  a  working  equilibrium  established.     The 


HYPER  TROPHY  &  DILA  TA  TION  OF  RIGHT  VENTRICLE.      3 1 7 

greater  the  regurgitation  or  stenosis  the  greater  the  amount 
of  hypertrophy  required  to  compensate  for  it.  The  change 
in  the  right  ventricle  thus  becomes,  together  with  the 
accompany  in  g  changes  in  the  left  ventricle,  a  measure  of 
the  regurgitation  or  stenosis. 

When,  therefore,  we  detect  a  mitral  murmur,  we  at  once 
examine  the  right  ventricle  in  order  to  gather  from  its  con- 
dition information  as  to  the  amount  of  reflux  or  obstruction 
which  is  not  yielded  by  the  murmur  itself.  This  is  specially 
the  case  when  symptoms  of  failing  compensation  have  set 
in.  But  if  the  right  ventricle  is  in  a  state  of  degeneration 
or  great  weakness,  as  may  be  the  case  in  lesions  established 
late  in  life,  these  indications  fail  us  altogether.  The 
absence  of  dilatation  and  hypertrophy,  instead  of  denoting 
comparatively  slight  regurgitation  or  stenosis,  shows  that 
the  right  ventricle  is  incapable  of  coping  with  it.  There  is 
no  right  ventricle  impulse,  and  the  pulmonic  second  sound 
instead  of  being  accentuated  is  weak,  while  dropsy  and  other 
evidences  of  serious  stasis  and  back  pressure  in  the  venous 
system  are  prematurely  developed  for  lack  of  hypertrophy 
or  compensatory  effort  on  the  part  of  the  right  ventricle. 

Under  these  circumstances  the  prognosis  is  extremely 
srrave.  The  risrht  ventricle  is  unable  to  come  to  the  aid  of 
the  left,  the  mechanism  of  compensation  makes  default, 
and  the  back  pressure  bears  at  once  upon  the  venous 
system.  The  fulcrum  for  some  of  our  most  efficacious 
therapeutic  measures  is  missing.  We  dare  not  open  a  vein 
however  great  the  respiratory  embarrassment  and  cyanosis  ; 
the  effect  of  leeching  over  the  liver  is  less  certainly  good, 
and  a  dose  of  calomel  is  not  well  borne.  Eecovery  is  rare, 
and  twice  it  has  happened  in  my  experience  that  during 
apparent  convalescence,  when  an  unfavourable  prognosis 
seemed  to  have  been  belied,  the  patient  has  died  suddenly 
when  beginning  to  walk  about,  and  the  right  ventricle  has 
been  found  degenerated  at  the  autopsy. 


3i 8  HEART  DISEASE. 

Similar  conditions  result  from  time  to  time  from  adhesion 
of  the  pericardium.  The  right  ventricle  suffers  proportion- 
ately more  than  the  left  from  pericarditis,  as  its  walls  are 
relatively  very  thin,  and  when  the  muscle  is  damaged  by 
myocarditis  the  ventricle  readily  dilates.  Again,  the  right 
ventricle  is  much  more  hampered  by  adhesion  of  the  peri- 
cardium than  the  left,  partly  because  its  superficial  area  is 
relatively  large,  but  chiefly  because  of  the  thinness  of  its 
walls ;  and  when  the  adhesions  are  general,  and  especially 
if  there  is  also  adherence  of  the  pericardium  to  the  chest 
wall  and  diaphragm,  efficient  contraction  of  this  ventricle 
must  be  impossible.  Cases  are  not  uncommon  in  which 
there  is  valvular  disease,  mitral  or  aortic,  but  from  the  size 
of  the  heart,  the  position  and  character  of  the  apex  beat 
and  impulse,  the  persistence  of  sounds  in  spite  of  the 
murmurs,  there  are  grounds  for  concluding  that  the  valvular 
lesion  is  not  very  severe.  There  is,  however,  a  premature 
development  of  symptoms.  Under  such  circumstances,  we 
may  often  confidently  infer  adhesion  of  the  pericardium 
when  it  cannot  be  demonstrated  with  any  certainty  by 
physical  signs.  This  has  already  been  discussed  in  the 
chapter  on  adherent  pericardium. 

The  right  ventricle  is  undoubtedly  sometimes  the  cause 
of  sudden  death,  and  when  the  heart  is  embarrassed  or 
stopped  by  pressure  upwards  of  the  diaphragm  by  a  dis- 
tended stomach  or  colon,  it  must  be  on  the  right  ventricle 
that  the  pressure  takes  effect.  This  part  of  the  heart  rests 
upon  the  diaphragm,  and  will  be  directly  compressed  when 
it  is  pushed  up.  Probably  it  is  the  diastole  which  is 
mostly  interfered  with,  and  it  would  seem  that  the  proper 
expansion  and  filling  of  the  ventricle  must  be  impossible 
when  the  pressure  upon  it  is  such  that  the  heart  is  carried 
up  bodily  by  the  diaphragm,  especially  when  the  ventricle 
is  dilated  and  over-distended.  A  melancholy  illustration 
of  this  occurred  in  my  experience  in  the  case  of  an  eminent 


HYPER  TROPHY  &>  DILA  TA  TION  OF  RIGHT  VENTRICLE.      3 1 9 

artist.  He  was  suffering  from  mitral  stenosis  and  regurgi- 
tation, and  had  overthrown  the  compensation  established  by- 
hypertrophy  of  the  right  ventricle  by  serious  imprudence  in 
the  form  of  over-exertion  and  exposure  undertaken  to  remedy 
the  effects  of  overwork.  There  was  an  extreme  degree  of  dis- 
tension of  the  right  side  of  the  heart,  with  tricuspid  regur- 
gitation, and  he  suffered  from  sleeplessness  and  dyspnoea, 
so  that  his  misery  was  insupportable,  and  life  was  despaired 
of.  The  application  of  leeches  over  the  liver,  which  was 
enormously  swollen,  and  the  administration  of  calomel,  at 
once  gave  him  sleep,  and  by  a  repetition  of  the  leeches  and 
regular  employment  of  mercurial  aperients,  with  the  usual 
heart  tonics,  he  so  far  recovered  as  to  be  able  to  leave  his 
room,  and  his  convalescence  seemed  to  be  assured. 

One  morning,  after  a  hearty  breakfast  in  bed,  the  nurse 
was  about  to  wash  his  face  and  hands  as  usual,  but  he 
impatiently  bade  her  give  him  the  basin,  and  stand  aside. 
He  sat  up  in  bed  with  the  basin  between  his  knees,  and 
when  the  time  came  for  washing  his  face,  bent  forwards  over 
it.  The  pressure  upwards  of  a  full  stomach  caused  by  this 
movement  brought  the  weak  right  ventricle  to  a  standstill, 
and  the  patient  fell  back  dead. 

One  cannot  help  being  reminded,  in  relating  this  incident, 
of  the  rough  and  ready,  but  effectual,  way  in  which  a  man 
is  brought  to  who  faints  after  the  severe  exertion  of  a 
boat  race.  He  is  seated  on  the  ground,  and  his  body  is 
bent  forcibly  forwards,  so  that  his  head  almost  comes  to  the 
ground  between  his  knees,  or,  if  he  has  fallen  forwards  over 
his  oar,  it  is  done  while  he  is  in  the  boat.  The  modus 
operandi  of  the  remedy  is  pressure  on  the  distended  right 
heart,  and,  when  emetics  are  resorted  to  in  bronchitis,  which 
has  gone  on  to  the  production  of  cyanosis,  the  good  effect  is 
due,  not  only  to  the  emptying  of  the  bronchial  tubes,  but 
to  unloading  of  the  right  auricle  and  ventricle  by  compres- 
sion in  the  act  of  vomiting. 


CHAPTER  XXII. 
DISEASE   OF   THE  CORONARY    ARTERIES. 

ATHEROMA     OE     SCLEROSIS — ENDARTERITIS — THROMBOSIS — 
EMBOLISM — ANEURYSM. 

Disease  of  the  coronary  arteries  is  very  common,  and  is  of 
the  first  importance,  inasmuch  as  they  constitute  the  sole 
blood  supply  to  the  heart,  and  obstruction  to  the  flow  of 
blood  through  them  from  disease  of  their  walls  may  be  a 
cause  of  sudden  death,  or  give  rise  to  degenerative  change 
in  the  cardiac  muscle  which  eventually  occasions  heart 
failure. 

Atheroma  or  sclerosis  is  the  commonest  affection  of  the 
coronary  arteries.  The  terms  "  atheroma  "  and  "  sclerosis  " 
are  employed  indiscriminately  to  denote  the  same  affection, 
though,  strictly  speaking,  atheroma  etymologically  means 
"  a  gruel-like  condition,"  and  sclerosis  "  a  hardening." 

Probably  this  confusing  nomenclature  has  originated 
from  the  presence  in  the  aorta  of  patches  of  softening  and 
ulceration,  whereas  arteries  when  affected  are  hard,  firm, 
and  inelastic  to  the  touch.  Hence  the  term  "  atheroma  " 
is  commonly  employed  to  denote  degenerative  changes  in 
the  aorta,  and  "  sclerosis "  similar  changes  in  the  smaller 
arteries.  Pathologically,  however,  and  to  a  great  extent 
etiologically,  the  conditions  are  identical. 

The  general  question  of  atheroma  is  discussed  in  a  later 
chapter.  For  the  present  we  are  chiefly  concerned  with 
the  effect  on  the  heart  of  degenerative  changes  in  the 
coronary  vessels. 


DISEASE   OF  THE   CORONARY  ARTERIES.  321 

Morbid  Anatomy. — The  coronary  arteries  are  thickened, 
inelastic,  and  hard.  Their  lumen  may  be  partially 
obstructed  by  small  whitish,  opaque  projections,  so  that  on 
section  they  have  the  appearance  of  a  signet  ring,  with  the 
signet  turned  inwards,  or  the  lumen  may  be  almost 
occluded  by  a  uniform  thickening  which  involves  the  whole 


FlO.  19a. — SECTION  OP  CORONARY  ARTERY  SHOWING  ADVANCED  SCLEROSIS.  A, 
GREATLY  THICKENED  INTIMA  ;  B,  INTERNAL  ELASTIC  LAMINA  ;  C,  MUSCULAR 
COAT  ;  D,  ADVENTITIA.  AT  X  THE  MUSCULAR  COAT  IS  ALMOST  DESTROYED, 
AND  PATCHES  OF  CALCIFICATION  ARE  SEEN  IN  THE  DEGENERATED  TISSUE 
BENEATH. 

circumference.  On  microscopic  examination  of  a  section 
through  one  of  these  projections,  it  is  seen  to  consist  of  a 
swelling  immediately  beneath  the  endothelium,  which  is 
pushed  inwards  ;  externally  it  is  usually  limited  by  the 
internal  elastic  lamina.  The  muscular  coat  beyond  this 
may  be  atrophied  from  pressure,  or  may  in  advanced  disease 
be  involved    in   the  degenerative  process  and   to  a  great 

Y 


322  HEART  DISEASE. 

extent  destroyed.  The  swelling  is  seen  to  consist  of 
amorphous  non-staining  debris,  in  which  may  be  distin- 
guished strands  of  hyaline  degenerated  tissue,  and  small 
atrophic  nuclei  of  cells  which  vary  greatly  in  number  in 
different  stages  of  the  disease.  (  Vide  Fig.  19a.)  Frequently 
calcareous  patches  are  present  from  deposit  of  lime  salts 
in  the  degenerated  tissue. 

The  condition  would  seem  to  suggest  necrosis  of  the 
subendothelial  tissue  either  from  toxic  influences  or  from 
imperfect  nutrition,  followed  by  swelling  of  the  necrotic 
tissue  and  a  futile  attempt  at  repair,  the  latter  being 
evidenced  by  the  presence  of  the  cellular  infiltration,  which 
appears  to  consist  of  atrophic  connective  tissue  cells. 

Huchard  regards  endarteritis  obliterans  of  the  vasa 
vasorum,  which  may  be  due  to  a  variety  of  causes,  as  the 
most  important  etiological  factor  in  this  primary  necrosis. 
Some  consider  that  proliferation  of  connective  tissue  cells 
beneath  the  endothelium  is  the  first  stage  in  the  process, 
occurring  as  a  result  of  irritation  due  to  intermittent  strain, 
or  to  some  toxic  substance,  and  that  necrosis  of  this  newly 
formed  tissue  follows.  Be  this  as  it  may,  the  important 
point  is,  that  narrowing  of  the  lumen  of  the  coronary 
arteries  and  its  branches  results,  and  consequently  obstruc- 
tion to  the  flow  of  blood  through  them ;  moreover,  even  in 
the  absence  of  pronounced  obstruction,  the  rigidity  and  loss 
of  elasticity  in  the  vessels  and  the  presence  of  calcareous 
plates  in  their  walls  seriously  impair  the  circulation  in 
the  heart.  Hence  may  result  sudden  death,  angina  pectoris, 
and  various  degenerative  changes  in  the  heart  muscle 
described  in  the  following  chapters. 

Endarteritis  obliterans  of  syphilitic  origin,  or  possibly 
due  to  other  toxins,  may  affect  the  coronary  arteries. 

In  this  affection  there  is  active  proliferation  of  the  cells 
of  the  endothelium  which  is  not  followed  by  degenera- 
tive changes,  so  that  there  is  uniform  thickening  of  the 


DISEASE   OF  THE   CORONARY  ARTERIES.  323 

vessel  with  narrowing  of  its  lumen,  and  actual  obliteration 
may  ensue  in  some  of  the  smaller  branches  of  the  coronary 
artery.  It  is  frequently  accompanied  by  periarteritis  or 
thickening  of  the  adventitia. 

Thrombosis. — This  usually  occurs  in  association  with 
sclerosis  of  the  coronary  arteries,  the  diseased  condition  of 
the  vessel  wall  and  the  narrowing  of  its  lumen  contributing 
to  the  result.  Obstruction  at  the  mouth  of  the  coronary 
artery  from  atheroma  of  the  aorta  involving  its  orifice,  or 
from  a  thrombus  attached  to  a  diseased  aortic  valve,  may 
also  be  a  contributory  factor.  Slowing  of  the  blood  stream 
in  a  failing  heart  is  also  an  important  cause. 

Infarction. — There  are  anastomoses  between  the  main 
trunks  of  the  coronary  arteries,  but  there  are  no  anasto- 
moses between  the  smaller  branches  after  they  have  entered 
the  myocardium.  The  intramuscular  branches  are  there- 
fore "terminal  arteries"  in  Cohnheim's  sense  of  the  word, 
and  infarction  results  when  they  are  occluded  by  thrombosis 
or  embolism. 

Infarcts  of  the  heart  are  not  typically  wedge-shaped,  as 
in  the  kidney  or  lung,  but  are  somewhat  irregular  in 
outline,  those  I  have  seen  being  oblong,  tapering  at  the 
distal  end.  They  are  usually  anaemic,  of  a  pale  yellowish 
colour,  sometimes  surrounded  by  a  zone  of  hyperemia. 
Microscopically  they  show  coagulation  necrosis  of  the 
portion  of  muscle  cut  off  from  its  blood  supply.  They 
may  break  down  and  give  rise  to  an  aneurism  or  to  rupture 
of  the  heart,  or  they  may  be  gradually  absorbed  and 
replaced  by  fibrous  tissue. 

Thrombosis  of  one  of  the  main  trunks  of  the  coronary 
artery  may  be  a  cause  of  rapid  death.  Cases  are,  however, 
on  record  which  show  that  thrombosis  of  a  large  branch 
may  occur  without  causing  death.  This  may  be  explained 
by  the  fact  that  there  are  anastomoses  between  the  main 
branches  of  the  coronary  arteries,  and  if  the  thrombosis  is 


324  HEART  DISEASE. 

gradual  in  onset,  sufficient  time  may  elapse  for  efficient 
collateral  circulation  to  be  established.  Much  will,  of  course, 
depend  on  the  size  of  the  thrombus  and  its  situation,  and 
whether  or  not  it  blocks  the  mouth  of  an  anastomosing 
branch. 

There  are  no  characteristic  physical  signs  or  symptoms 
by  which  thrombosis  of  the  coronary  vessels  can  be 
diagnosed. 

It  is  probably  of  much  commoner  occurrence  than  is 
generally  supposed,  and  it  is  possible  that  it  may  cause 
attacks  of  angina  pectoris  or  precordial  pain,  and  be 
responsible  for  a  certain  proportion  of  cases  of  sudden 
death  which  are  put  down  to  other  causes,  such  as  fatty 
degeneration  of  the  heart,  etc.  A  systematic  investigation 
of  the  coronary  arteries  throughout  their  course  is  not 
commonly  made  at  post-mortem  examinations,  and  my 
attention  was  drawn  to  the  subject  in  investigating  a  case 
of  Bright's  disease  in  which  the  heart  was  enormously 
hypertrophied,  where  I  found  two  infarcts  in  the  wall  of 
the  left  ventricle,  with  extensive  thrombosis  of  two  branches 
of  ihe  left  coronary  artery.  The  thrombosis  was  not  evident 
till  I  laid  open  the  walls  of  the  vessel  throughout  their 
course  in  searching  for  an  explanation  of  the  infarcts.  The 
patient  died  from  uraemia,  and  not  from  the  coronary 
thrombosis,  which  from  the  microscopic  appearances  of  the 
infarcts  had  apparently  taken  place  some  little  time 
before. 

Embolism. — This  is  far  less  common,  according  to  Welch,* 
than  thrombosis.  It  may  occur  in  pernicious  endocarditis 
from  detachment  of  a  fragment  of  an  affected  valve,  or 
possibly  in  atheromatous  degeneration  of  the  aorta,  from 
detachment  of  a  portion  of  a  thrombus  adherent  to  the 
diseased  surface.  Embolism  of  the  coronary  arteries  gives 
rise  to  results  similar  to  those  of  thrombosis  described 
*  Allbutt's  "  System  of  Medicine,"  vol.  vi.  p.  281. 


DISEASE   OF  THE   CORONARY  ARTERIES.  325 

above,  namely,  sudden  death  or  infarction,  according  as  a 
main  branch  or  an  intramuscular  branch  is  affected  ;  but 
whereas  death  due  to  thrombosis  may  be  preceded  by  pre- 
monitory symptoms  from  the  more  gradual  nature  of  the 
onset  of  thrombosis,  death  due  to  embolism  must,  when  it 
occurs,  be  absolutely  sudden. 

Aneurysm  of  the  coronary  arteries  is  rare.  It  may 
result  from  local  weakening  of  the  vessel  by  atheroma  or 
syphilitic  disease,  or  from  acute  softening  of  the  arterial 
wall  due  to  lodgment  of  septic  emboli  on  its  inner  aspect 
in  pernicious  endocarditis. 

Huchard*  gives  an  account  of  eleven  cases  which  he  has 
collected  from  international  literature.  In  all  except  two 
the  aneurysms  were  associated  with  atheromatous  degenera- 
tion of  the  coronary  vessels.  In  the  remaining  two  the 
patients  were  young,  21  and  22;  the  aneurysms  were 
multiple ;  pyrexia  was  present  in  one  case  of  obscure  origin, 
in  the  other  the  patient  had  suffered  from  malarial  fever. 
In  nine  of  the  cases  sudden  death  occurred  from  rupture  of 
the  coronary  aneurysm. 

In  the  St.  Mary's  Hospital  Museum  is  a  specimen  with 
thirteen  small  aneurysms  of  the  coronary  artery  of  embolic 
origin,  from  a  case  of  pernicious  endocarditis  in  a  girl  aged 
ten. 

There  are  no  symptoms  or  physical  signs  by  which 
aneurysm  of  the  coronary  arteries  can  be  diagnosed  during 
life.  They  must,  however,  necessarily  impair  the  circulation 
in  the  heart,  and  most  commonly  they  rupture  and  cause 
sudden  death. 

*  "  Mai.  du  Coeur,"  vol.  i.  pp.  232  et  seq. 


CHAPTER   XXIII. 
AFFECTIONS    OF   THE    MYOCARDIUM. 

ACUTE  MYOCARDITIS  —  FIBROID  CHANGE  — ETIOLOGY  AND 
MORBID  ANATOMY — SYPHILITIC  AFFECTIONS  OF  THE 
MYOCARDIUM  — PHYSICAL  SIGNS  AND  SYMPTOMS  OF 
FIBROSIS  —DIAGNOSIS—  PROGNOSIS  — TREATMENT. 

Acute  interstitial  myocarditis  occurs  most  commonly  in 
association  with  pericarditis  or  endocarditis.  It  is  not 
simply  due  to  direct  extension  of  the  inflammatory  process 
from  the  pericardium  or  endocardium  along  the  connective 
tissue  network  to  the  subjacent  muscular  substance,  but, 
as  Poynton  *  has  shown,  in  rheumatic  pericarditis  and 
endocarditis  there  is  usually  a  general  "carditis,"  a  term 
suggested  by  the  late  Dr.  Sturges,  and  implying  inflam- 
mation of  the  heart  throughout  its  substance. 

Morbid  Anatomy. — The  inflammatory  changes  are  usually 
best  marked  in  cases  of  subacute  pericarditis  that  prove 
fatal.  On  microscopic  examination,  the  nuclei  in  the  inter- 
stitial tissue  are  seen  to  be  increased  in  number  owing  to 
exudation  of  leucocytes  between  the  muscle  fibres  and  pro- 
liferation of  the  connective  tissue  cells.  In  pernicious 
endocarditis  large  masses  of  micrococci,  surrounded  by  an 
inflammatory  zone  of  polynuclear  leucocytes,  may  some- 
times be  seen  in  the  substance  of  the  heart  wall  as  shown 
in  the  illustration  (Fig.  20),  where  the  muscle  fibres  in 
the   neighbourhood   are   destroyed   and   broken   up.      The 

*  Med.  Chi.  Trans.,  May,  1899. 


ACUTE  MYOCARDITIS. 


327 


muscular  fibres  are  affected  iu  varying  degree,  those  near 
the  surface,  as  a  rule,  more  than  those  in  the  deeper  layers. 
Of  some,  nothing  will  remain  but  a  mass  of  granular 
material ;  others  have  lost  their  striation,  and  are  swollen 
and  opaque;  others  are  in  a  state  of  cloudy  swelling,  and 
some  may  appear  to  be  little  altered.  The  changes  will 
be  more  marked  and  general  in  proportion  to  the  duration 
and  severity  of  the  inflammation. 


FIG.  20. — SECTION  OP  HEART  MUSCLE  FROM  A  CASE  OF  PERNICIOUS  ENDO- 
CARDITIS, SHOWING  ACUTE  INTERSTITIAL  MYOCARDITIS.  MASSES  OF 
MICRO-ORGANISMS  ARE  SEEN  AT  A,  A,  A,  AND  THERE  IS  'WIDESPREAD 
INFILTRATION  OF  POLYNUCLEAR  LEUCOCYTES  WITH  DESTRUCTION  OF 
MUSCLE   FIBRES. 


Physical  Signs. — In  the  early  stages,  acute  myocarditis 
gives  rise  to  no  definite  physical  signs  or  symptoms  by 
which  its  existence  can  be  diagnosed  with  any  degree  of 
certainty.  When  present,  the  physical  signs  will  be  those 
indicative  of  progressive  cardiac  dilatation  or  asthenia,  or 
of  both  combined.  The  signs  of  cardiac  dilatation  will  be, 
increase  in  the  area  of  cardiac  dulness  with  displacement  of 
the  apex  beat  downwards  and  outwards,  and  weakening  of 


328  HEART  DISEASE. 

the  first  sound,  the  impulse  becoming,  at  the  same  time, 
diffuse  and  tapping  in  character.  The  signs  of  cardiac 
asthenia  will  be  feebleness  or  loss  of  the  apex  beat,  with 
weak  and  short  heart  sounds,  and  a  frequent,  short,  and 
easily  compressible  pulse.  When  acute  myocarditis  occurs 
in  association  with  pericarditis  of  rheumatic  origin,  the 
cardiac  dilatation  is  rapid  and  considerable,  and  signs  of 
cardiac  weakness  and  embarrassment  appear  early  in  the 
course  of  the  disease. 

Prognosis. — The  prognosis  depends  on  the  extent  to  which 
the  cardiac  muscle  is  affected  by  the  inflammatory  process. 
Myocarditis  is,  however,  almost  invariably  associated  with 
pericarditis  or  endocarditis,  affecting  the  prognosis  in  these 
affections  very  materially.  This  has  already  been  referred 
to  in  the  chapter  on  pericarditis,  where  the  prognosis  of 
the  combined  affections  is  fully  discussed.  After  the  acute 
attack  has  subsided,  the  muscle  fibres  which  have  been 
destroyed  are  replaced  by  fibrous  tissue,  which  leads  to 
serious  weakening  of  the  heart  wall.  Consequently,  the 
heart  will  be  liable  to  break  down  under  any  unusual 
exertion,  and  the  various  symptoms  associated  with  fibroid 
changes  in  the  heart  walls  may  set  in  at  a  later  period. 

Treatment. — There  is  no  special  treatment  beyond  that 
for  the  pericarditis  and  rheumatism  usually  associated 
with  it. 

Cloudy  Swelling. — Under  the  head  of  myocardial  in- 
flammation are  included  the  changes  in  the  cardiac  muscle, 
known  as  "  cloudy  swelling,"  or  albuminoid  degeneration, 
which  occur  in  certain  diseases  attended  by  high  and  pro- 
longed fever,  such  as  septicseinia,  pneumonia,  enteric  fever, 
scarlet  fever,  rheumatism,  etc.  Cloudy  swelling  is  not 
confined  to  the  heart,  but  is  found  at  the  same  time  in  the 
liver,  kidney,  and  spleen,  and  appears  to  be  due,  mainly, 
if  not  entirely,  to  toxins  evolved  by  the  micro-organisms 
which  are  responsible  for  the  disease.     The  changes  differ 


CLOUDY  SWELLING.  329 

from  those  found  in  acute  interstitial  myocarditis  just 
described,  inasmuch  as  they  are  mainly  confined  to  the 
muscular  fibres. 

Morbid  Anatomy. — The  interstitial  tissue  is  not  as  a 
rule  affected,  though  some  cellular  exudation  may  be 
present,  the  changes  being  chiefly  manifest  in  the 
muscle  fibres.  These  are  swollen,  their  striation  is  indis- 
tinguishable, and  they  are  rendered  opaque  by  the  fine 
granules  which  pervade  their  substance  and  obscure  their 
nuclei.  The  granules  are  composed  of  an  albuminoid 
material,  soluble  in  acetic  acid,  after  treatment  with  which 
the  muscular  fibres  seem  to  almost  regain  their  normal 
appearance.  The  condition  of  cloudy  swelling  is  frequently 
followed  by  fatty  degeneration  of  the  muscle  fibres,  if  the 
fever  is  prolonged  or  the  toxaemia  is  severe. 

Physical  Signs  and  Symptoms. — The  physical  signs  and 
symptoms  are  those  of  progressive  cardiac  asthenia.  The 
first  sound  of  the  heart  becomes  gradually  weaker  and 
shorter,  and  the  apex  beat  more  and  more  feeble  till  it  is 
scarcely  perceptible.  There  is  seldom  any  marked  dilata- 
tion of  the  ventricles  in  the  earlier  stages,  as  is  the  case 
in  the  interstitial  myocarditis  of  rheumatism.  The  pulse 
is  increased  in  frequency,  easily  compressible,  and  often 
markedly  dichrotic. 

Prognosis. — The  prognosis  is  that  of  the  disease  to  which 
the  cardiac  condition  is  secondary. 

Treatment. — Stimulants  such  as  brandy  or  ether  may  be 
necessary,  together  with  strychnine,  which  is  usually  more 
effective  when  given  hypodermically.  Sometimes  digitalis 
in  small  doses  is  of  benefit  during  convalescence,  but  it 
should  not  be  given  while  fever  is  present,  as  the  damaged 
muscle  fibres  are  not  in  a  condition  to  profit  by  increase  of 
tone,  and  the  increase  of  peripheral  resistance  would  entail 
more  work  on  the  heart. 


33°  HEART  DISEASE. 


Fibroid  Change  in  the  Heart  Walls. 

Two  main  varieties  of  fibroid  change  in  the  heart  wall 
may  be  distinguished — 

(1)  A  substitution  of  fibrous  tissue  for  muscle  fibres 
which  have  been  damaged  or  destroyed  by  disease. 

(2)  A  patchy  or  diffuse  fibrosis  of  the  heart  associated 
with  marked  degenerative  changes  in  the  coronary  vessels. 
The  question  as  to  whether  this  fibroid  change  is  a  direct 
result  of  disease  of  the  coronary  vessels,  or  whether  it  is  the 
result  of  a  chronic  interstitial  inflammation,  or  whether 
some  of  these  cases  should  be  classified  in  Group  I.,  will 
be  discussed  later. 

Etiology. — 1.  In  the  process  of  repair,  cicatricial  fibrous 
tissue  may  take  the  place  of  muscle  fibres  destroyed  by 
acute  myocarditis  due  to  some  acute  bacterial  infection, 
by  gummata,  or  by  acute  softening  the  result  of  embolism 
or  thrombosis  of  branches  of  the  coronary  arteries. 

Huchard  *  gives  a  remarkable  illustration  of  areas  of 
dense  fibrosis  in  the  heart  wall,  produced  experimentally  by 
Mollard,f  by  repeated  inoculations  of  diphtheria  toxin, 
the  fibrous  tissue  having  been  formed  in  the  process 
of  repair  to  replace  the  muscle  fibres  which  have  been 
destroyed  by  the  toxin.  This  important  experimental 
evidence  shows  that  acute  toxaemias  may  be  responsible,  if 
the  patient  recovers,  for  areas  of  dense  patchy  fibrosis,  which 
later  on  may  give  rise  to  apparently  unaccountable  symptoms 
of  myocardial  weakness.  In  a  very  extreme  case  of  fibrosis 
of  the  heart,  which  I  mounted  for  the  St.  Mary's  Hospital 
Museum,  and  which  is  figured  in  the  text  (Fig.  21),  about 
two-thirds  of  the  heart  wall  consists  of  dense  fibrous  tissue. 
The  endocardium  was  also  of  a  dense  white  opaque  colour, 

*  "  Maladies  du  Cceur,"  vol.  i.  p.  214. 

|  "  Sclerose  du  Myocarde,"  Ann.  de  VInstitut  Pasteur,  18D7. 


FIBROSIS  OF  THE  MYOCARDIUM.  331 

and  the  mitral  valve  were  thickened  and  rigid,  though  there 


FIG.    21.— HEART   SHOWING   AN    EXTREME   DEGREE   OF   FIBROSIS 
OF   THE   WALLS   AND   ENDOCARDIUM. 

was  no  actual  loss  of  substance.     The  coronary  arteries  were 
patent,  and  not  rigid  or  thickened.     The  heart  was  dilated, 


332  HEART  DISEASE. 

but  not  hypertrophied.  Microscopically,  the  white  opaque 
tissue,  of  which  the  bulk  of  the  heart  wall  consists,  was  seen 
to  consist  of  very  dense  old  fibrous  tissue,  in  which  here  and 
there  were  seen  muscular  fibres  isolated  from  their  fellows, 
some  in  a  fair  state  of  preservation.  The  vessels  were  not 
obliterated  or  markedly  narrowed.  The  condition  suggests 
that  this  cicatricial  fibrous  tissue  has  replaced  muscular 
fibres  destroyed  at  one  time  by  a  severe  toxaemia,  possibly 
the  result  of  acute  endocarditis,  with  accompanying  myocar- 
ditis. The  heart  was  obtained  from  a  woman  aged  61,  who 
was  brought  in  dead  to  St.  Mary's  Hospital,  having  suc- 
cumbed to  a  sudden  syncopal  attack.  Unfortunately, 
therefore,  no  history  could  be  obtained. 

2.  Weigert  drew  attention  to  what  he  considers  an  im- 
portant cause  of  fibroid  changes  in  the  heart  wall,  namely, 
sclerosis  of  the  coronary  arteries.  He  states  that  when  the 
cardiac  circulation  is  slowly  interfered  with  by  sclerosis  of 
the  coronary  arteries,  atrophy  of  the  muscle  fibres  takes 
place  without  destruction  of  connective  tissue,  and  that 
the  shrunken  and  atrophied  fibres  are  gradually  replaced 
by  fibrous  tissue. 

Huchard  *  also  considers  that  obliterative  lesions  or 
endarteritis  of  the  coronary  arteries  are  the  most  common 
cause  of  patchy  fibrosis,  or,  as  he  terms  it,  of  "sclerose 
dystrophique."  He  holds  that  the  fibrosis  is  the  result  of 
a  primary  degenerative  change  in  the  muscle  fibres  due  to 
their  deprivation  of  nutriment,  and  that  this  necrosis  of 
the  muscle  fibres  sets  up  an  irritative  proliferation  in  their 
neighbourhood,  with  resulting  formation  of  fibrous  tissue. 
He  gives  illustrations  f  of  patchy  fibrosis  in  the  heart 
wall  with  obliterated  vessels  in  their  neighbourhood,  and 
states  that  "  there  is  never  well-marked  sclerosis  without 
accompanying  endarteritis."  % 

*  "Maladies  du  Cceur,"  vol.  i.  t  Ibid.,  pp.  215,  240,  241. 

X  Ibid.,  p.  242. 


FIBROSIS  OF  THE  MYOCARDIUM.  333 

He  considers  that  a  diagnosis  can  be  made  between  chronic 
myocarditis  and  what  he  terms  "  sclerose  dystrophique."  In 
both  affections  symptoms  of  myocardial  weakness  will  be 
a  prominent  feature,  namely,  dyspnoea  on  exertion,  feeble- 
ness of  the  apex  beat  and  the  first  sound,  enlargement  of  the 
area  of  cardiac  dnlness,  and  perhaps  congestion  of  the  bases 
of  the  kings  from  dilatation  and  back  working.  Certain 
symptoms,  however,  will  be  peculiar  to  "sclerose  dystro- 
phique," for  inasmuch  as  it  is  due  to  sclerosis  of  the  cardiac 
vessels,  there  will  be  evidence  of  vascular  degeneration  else- 
where, or  of  high  arterial  tension,  which  is  usually  associated 
with  it,  namely,  thickening  of  the  radials,  dilatation  of  the 
aorta,  tortuous  degenerated  brachials,  and  possibly  cerebral 
haemorrhage  may  occur. 

In  addition,  there  may  be  angina  pectoris  from  the 
narrowing  of  the  coronary  arteries. 

Lindsay  Steven,*  in  a  paper  on  the  subject,  gives  a 
series  of  twenty-one  cases  of  cardiac  fibrosis,  which  bear 
out  Weigert's  observations,  and  in  a  later  communication, f 
discussing  the  difficult  question  as  to  why  obstruction 
to  the  coronary  circulation  should  in  some  cases  give  rise  to 
fatty  degeneration  and  in  others  to  fibrosis,  comes  to  the 
following  conclusion  : — 

"  In  cases  where  the  main  coronary  artery  is  slowly 
obstructed,  and  at  last  completely  occluded  at  its  origin, 
generalized  fatty  degeneration  is  likely  to  occur,  and  the 
cause  is  similar  to  that  in  profound  anaemia,  namely, 
deterioration  in  the  supply  of  blood  to  the  whole  organ. 

"  When  smaller  branches  are  slowly  obstructed  but  the 
main  branches  remain  patent,  slight  fatty  degeneration 
may  result  with  localized  fibrosis." 

He  bases  his  conclusions  on  a  study  of  twenty-one  cases, 
in  nine  of  which  fatty  degeneration  was  present  as  well  as 
fibrosis.  In  nearly  all  his  cases  the  heart  was  hypertrophied, 
*  Journal  of  Path,  and  Bact.,  1894.  f  Lancet,  1887,  vol.  ii. 


334  HEART  DISEASE. 

nd  in  nine  there  was  chronic  interstitial  nephritis  and  in 
seven  atheroma  of  the  aorta. 

It  is  easy  to  conceive,  and  we  have  ample  evidence  that 
sclerosis  of  the  coronary  arteries  may  give  rise  to  fatty 
degeneration  and  atrophy  of  the  muscle  fibres  by  interference 
with  their  nutrition,  but  it  is  difficult  to  understand  how  it 
can  give  rise  to  fibrosis,  though  the  two  conditions  are 
undoubtedly  very  frequently  associated.  Huchard  considers 
that  the  narrowing  of  the  coronary  arteries  causes  death  of 
the  muscle  fibres  supplied  by  its  terminal  branches,  and 
that  this  necrobiosis  sets  up  an  irritative  inflammation  in 
the  adjoining  areas. 

Some  authors  consider  that  fibroid  change  in  the  heart 
is  the  result  of  chronic  inflammation.  Bristowe  applied 
the  term  "cirrhosis"  of  the  heart  to  this  condition,  and 
Friedreich  and  Lancereaux  speak  of  chronic  interstitial 
myocarditis  as  responsible  for  cardiac  fibrosis. 

Gibson  *  includes  under  the  head  of  chronic  myocarditis 
all  conditions  in  which  there  is  general  or  local  increase  of 
fibrous  tissue  in  the  myocardium.     Among  the  causes  he 

includes — 

(1)  Factors  modifying  the  condition  of  the  blood,  e.g. 
lithoemia,  glycsemia,  and  faulty  conditions  of  the  blood 
arising  from  defective  metabolism. 

(2)  Infective  diseases  such  as  enteric  fever,  also 
syphilis. 

(3).  All  changes  in  the  coronary  arteries,  whether  affecting 
their  walls  or  lumen. 

Huchard  considers  that  a  true  chronic  interstitial 
myocarditis  is  rare,  if,  indeed,  it  occurs,  as  he  holds  that 
destruction  of  muscle  fibres  precedes  fibrosis,  and  that  this 
is  most  commonly  dependent  on  sclerosis  of  the  coronary 
vessels. 

In  examining  hypertrophied  hearts  from  cases  of 
*  "Diseases  of  the  Heart  and  Aorta,"  p.  681. 


FIBROSIS  OF  THE   MYOCARDIUM.  335 

Bright's  disease,  in  which  there  was  slight  diffuse  interstitial 
change  or  fibrosis,  I  have  found  that  the  most  marked 
change  was  in  the  muscle  fibres,  namely,  swelling,  absence 
of  staining,  and  breaking  up  of  the  nuclei  (karyorhexis),  as 
in  Fig.  22,  at  the  poles  of  which  in  the  muscle  fibres  were 
granules  of  brown  pigment,  similar  to  those  seen  in  brown 
atrophy  of  the  heart.  In  these  cases  death  had  occurred 
from  cerebral  liEeinorrhage,  and  not  from  heart  failure. 

In  other  cases  of  hypertrophied  hearts  associated  with 


FIG.  22. — SECTION  OP  MUSCLE  FROM  HYPERTROPHIED  HEART,  SHOWING 
SWELLING,  LOSS  OP  STAINING  REACTION,  AND  BREAKING  UP  OF  NUCLEI, 
WITH   DEPOSIT   OF   GRANULES    OF   BROWN   PIGMENT    AT   THEIR   POLES. 


high  arterial  tension  and  general  arterio-sclerosis,  not  attri- 
butable to  Bright's  disease,  in  which  death  occurred  from 
heart  failure,  I  have  found  similar  changes  in  the  muscle 
fibres,  with  areas  of  patchy  fibrosis,  as  seen  in  Fig.  23. 
These  would  come  under  Huchard's  category  of  "sclerose 
dystrophique,"  as  they  were  associated  with  atheroma  of 
the  coronary  arteries  and  general  arterio-sclerosis. 

Possibly,  in  some  cases  of  cardiac  fibrosis  associated  with 
atheroma  of  the   coronary  arteries,  destruction  of   muscle 


336  HEART  DISEASE. 

fibres  and  substitution  of  fibrous  tissue  for  them  occurs  at 
an  earlier  date  than  the  degenerative  changes  in  the 
vessels,  as  a  result  of  some  acute  toxsemia.  Later  on  the 
vessels  are  affected,  and  sclerosis  of  the  coronary  arteries 
takes  place,  which  would  tend  to  cause  fatty  degeneration 
in  muscle  fibres  previously  undamaged,  and  thus  explain 
the  presence  of    fibrosis  and   fatty  degeneration   side    by 


/   t   ' 


I      ■ 


J    - 


:^J«< 


FIG.   23.  — SECTION    OF   HEART   WALL,  SHOWING   AREA    OP   FIBROSIS   ASSOCIATED 
WITH   ATHEROMA   OF   THE   CORONARY   ARTERIES. 


side  in  the  same  heart,  as  drawn  attention  to  by  Lindsay 
Steven. 

It  is  probable  that  syphilis  is  an  etiological  factor  in  a 
certain  proportion  of  cases,  fibrosis  resulting  either  from 
cicatrization  of  gummata,  or  possibly  occurring  in  association 
with  endarteritis  and  periarteritis  of  the  coronary  vessels. 

The  illustration  (Fig.  24)  is  a  striking  instance  of 
fibrosis  associated  with  extreme  narrowing  of  the  smaller 


FIBROSIS  OF    THE    MYOCARDIUM.  337 

branches  of  the  coronary  arteries,  the  lumen  of  which  was 
almost  obliterated.  The  specimen  came  from  a  woman 
aged  37,  who  died  suddenly.  The  heart  was  hypertrophied, 
and  the  aorta  was  atheromatous,  but  there  was  no  kidney 
disease.  The  age  of  the  patient  and  the  condition  of  the 
vessels,  which  is  that  of  endarteritis  obliterans,  strongly 
suggest  syphilis  as  the  cause. 

Syphilitic   affections   of   the   heart    wall   are   not    very 


'•—    /j® 


FIG.  24. — SECTION    OF    HEART   WALL,    SHOWING   FII5R0SIS   ASSOCIATED    WITH 
ENDARTERITIS   OBLITERANS   PROBABLY   OF   SYPUfLITIC   ORIGIN. 


common,  but  are  doubtless  frequently  overlooked.  Sidney 
Phillips,*  in  a  paper  on  this  subject,  recorded  twenty-five 
cases  described  by  various  authors,  together  with  some 
which  had  come  under  his  own  observation.  In  the  majority 
of  these  cases  gummata  were  the  lesions  found,  and  the 
diagnosis  was  only  made  on  the  post-mortem  table. 

Physical  Signs  and  Symptoms. — In  cases  associated  with 
coronary  sclerosis  and  general  vascular  degeneration,  the 

*  Lancet,  1897,  vol.  i.  p.  223. 

Z 


338  HEART  DISEASE. 

patient,  usually  middle-aged  or  elderly,  may  complain  of 
breathlessness,  palpitation,  precordial  oppression,  or  of 
anginoid  pains.  He  will  usually  be  a  man  who  lias  lived 
well,  or  who  has  led  an  arduous  and  strenuous  life.  The 
arterial  tension  will  be  high  and  the  radial  vessel  thickened 
somewhat.  The  heart  will  be  hypertrophied  to  a  varying 
degree.  There  will  usually  be  breathlessness  on  exertion, 
and  possibly  slight  oedema  of  the  legs,  which  subsides  after 
a  night's  rest  in  bed.  The  pulse  may  be  irregular,  and 
the  arterial  tension  moderate  or  low,  because  of  the  failing 
power  of  the  heart.  A  sudden  syncopal  attack  may  prove 
fatal  before  any  symptoms  of  a  nature  to  cause  anxiety 
have  arisen.  This  is  especially  liable  to  occur  in  cases 
where  there  is  marked  narrowing  of  the  coronary  arteries  or 
rigidity  due  to  degenerative  changes,  and  the  sudden  death 
is  to  be  attributed  to  this  cause  and  resulting  ischemia  of 
the  heart  rather  than  to  the  fibroid  changes  in  the  cardiac 
muscle.  Cerebral  haemorrhage  is  liable  to  occur,  as  degene- 
rative changes  are  frequently  present  in  the  cerebral  vessels. 
Cheyne-Stokes  respiration  may  develop  in  association  with 
this,  and  is  often  pronounced  and  persistent. 

In  other  cases  there  may  be  distressing  dyspnoea  at 
night  of  the  type  of  uraemic  asthma. 

When  cardiac  fibrosis  is  the  result  of  cicatrization  after 
damage  to  the  muscle  by  some  severe  toxaemia,  there  may  be 
at  a  later  date  dilatation  of  the  heart,  for  which  there  is  no 
apparent  cause ;  dropsy  may  set  in,  with  engorgement  of  the 
lungs  and  other  symptoms  of  back  working  and  right 
ventricle  failure,  and  the  condition  of  cardiac  fibrosis  is  not 
suspected  during  life. 

Diagnosis. — As  may  be  gathered  from  what  has  been 
previously  said,  the  diagnosis  of  this  condition  is  one  of 
considerable  difficulty,  and  is  to  a  great  extent  a  matter  of 
inference  during  life,  and  can  only  be  determined  with 
certainty  by  a  post-mortem  examination.     When,  however, 


FIBROSIS  OF  THE  MYOCARDIUM.  3j9 

in  association  with  evidence  of  vascular  degeneration,  the 
heart  is  hypertrophied,  and  there  are  breathlessness,  anginal 
pains,  a  tendency  to  syncopal  or  apoplectiform  attacks, 
with  a  failing  pulse,  one  may  suspect  fibrosis ;  but  there  are 
no  characteristic  features  by  which  this  can  be  diagnosed 
from  other  degenerative  changes  in  the  heart  muscle. 

Prognosis. — This  is  necessarily  unfavourable,  inasmuch 
as  cardiac  fibrosis  is  usually  associated  with  degenerative 
changes  in  the  vascular  system  as  a  whole,  and  in  the 
coronary  and  cerebral  vessels  in  particular.  Because  of 
the  associated  sclerosis  of  the  coronary  arteries,  death  may 
result  from  sudden  syncope  without  previous  warning,  or 
anginal  attacks  may  set  in,  one  of  which  eventually  proves 
fatal.  Cerebral  haemorrhage  is  liable  to  occur,  giving  rise 
to  hemiplegia,  and  is  frequently  associated  with  Cheyne- 
Stokes  respiration  of  a  pronounced  and  distressing  type. 
This  may  develop  in  the  absence  of  cerebral  haemorrhage, 
and  is  always  of  serious  prognostic  significance. 

Frequency  or  irregularity  of  pulse  usually  are  un- 
favourable indications,  if  persistent,  and  not  due  to  reflex 
causes;  but  in  one  case  in  which  irregularity  was  present 
to  a  marked  degree,  with  breathlessness  on  exertion  and 
slight  cedeina  of  the  legs,  the  patient,  after  a  month's  rest 
in  bed,  regained  his  health,  and  by  care  in  his  mode  of 
life  survived  for  six  years,  though  the  pulse  remained 
irregular  all  the  time.  Eventually  he  succumbed  to  a 
sudden  syncopal  attack. 

In  another  case,  apparently  similar  at  the  outset,  the 
patient,  three  months  after  he  sought  medical  advice,  had 
an  attack  of  cerebral  hsemorrhage,  associated  with  Cheyne- 
Stokes  respiration.  He  began  to  recover  some  power  in 
the  affected  side,  but  a  month  later  had  another  attack  of 
cerebral  hemorrhage,  which  proved  fatal. 

Possibly,  in  fibrosis  associated  with  syphilitic  endarte- 
ritis, the  prognosis  is  more  favourable  if  an  early  diagnosis 


34°  HEART  DISEASE. 

could  be  made  and  suitable  treatment  carried  out,  but  this 
is  scarcely  possible  in  the  majority  of  cases,  and  even  on 
careful  microscopic  examination  post-mortem  it  is  difficult 
to  be  sure  of  a  syphilitic  origin. 

According  to  the  statistics  of  the  cases  collected  by 
Sidney  Phillips,  gummata  usually  give  rise  to  no  definite 
physical  signs  or  symptoms,  and  death  is  liable  to  occur 
from  a  sudden  syncopal  attack,  or  possibly  rupture  of  the 
heart.  Aneurysm  of  the  heart  may  be  a  result  of  a  gumma, 
or,  in  the  most  favourable  cases,  cicatrization,  with  a  result- 
ing patch  of  fibrosis. 

Apart  from  syphilis,  the  cases  in  which  the  prognosis  is 
most  favourable  are  those  in  which  the  fibrosis  is  the  result 
of  cicatrization  after  damage  to  the  heart  muscle  by  acute 
myocarditis.  It  is  probable  that  in  many  cases  no  symptoms 
arise  until  later  on  in  life,  when  possibly  degenerative  changes 
may  set  in  in  the  previously  undamaged  muscle,  associated 
with  sclerosis  of  the  coronary  vessels.  In  other  cases, 
Avhere  the  lesion  is  severe,  cardiac  dilatation  may  result, 
for  which  there  is  no  apparent  cause,  and  which  resists  all 
treatment,  and  it  is  only  on  careful  microscopical  examina- 
tion of  the  heart  muscle  post  mortem  that  the  explanation 
is  manifest. 

Treatment. — This  must  be  directed  to  relieving  the  heart 
of  work  as  far  as  possible.  Moderation  in  food  and  drink, 
and  regularity  of  meals  must  be  enjoined,  to  avoid  undue 
variations  of  blood  pressure  ;  and  measures  must  be  taken 
for  the  lowering  of  arterial  tension  if  this  be  excessive. 
For  this  purpose  mercurial  purgatives  combined  with  colo- 
cynth  and  hyoscyamus  should  be  given  once  a  week,  or 
oftener  if  required,  and  vaso-dilators,  such  as  erythrol 
tetranitrate  or  liquor  trinitrin,  should  be  administered,  and 
continued  for  a  long  period  if  necessary.  Rest  in  bed  must 
be  insisted  on  when  warning  symptoms  such  as  breathless- 
ness  on  slight  exertion,  or  oedema  of  the  extremities  are 


FIBROSIS  OF  THE  MYOCARDIUM.  341 

present.  Iodide  of  potassium  is  useful  not  only  in  syphilitic 
fibrosis,  but  in  all  cases  where  there  is  general  thickening 
of  the  arteries  and  evidence  of  atheroma.  Cardiac  tonics, 
such  as  strychnine,  mix  vomica,  and  arsenic,  may  often  be 
given  with  marked  benefit,  but  digitalis  and  its  congeners 
are  seldom  indicated. 


CHAPTER  XXIV. 

AFFECTIONS  OF  THE  MYOCARDIUM  (Continued). 

distinction  between  fatty  infiltration  of  obesity 
and  fatty  degeneration — causation  of  fatty 
degeneration  —  symptoms  —  spontaneous  rupture 
of  the  heart — physical  signs — diagnosis — prog- 
nosis— treatment — aneurysm  and  new  growths 
of  the  heart. 

Fatty  Degeneration. 

No  form  of  heart  disease  is  regarded  with  so  much  appre- 
hension as  fatty  degeneration.  More  than  any  other,  it 
carries  with  it  the  danger  of  sudden  death  and  the  liability 
to  angina  pectoris,  and,  although  happily  it  is  not  very 
common,  it  would  be  a  most  important  acquisition  to  be 
able  to  make  the  diagnosis  with  certainty  at  an  early 
period. 

It  must  be  understood  from  the  first  that  fatty  infiltra- 
tion or  the  fat-laden  heart  of  obesity  does  not  come  under 
the  designation  of  fatty  degeneration,  and  it  may  be  dis- 
missed from  further  consideration  with  a  few  words.  In 
advanced  life  there  is  a  tendency  to  the  formation  of  adipose 
tissue  beneath  the  visceral  pericardium,  especially  along 
the  course  of  the  coronary  arteries.  In  obese  persons  and 
those  addicted  to  alcohol,  more  especially  beer  drinkers, 
the  amount  may  become  considerable,  so  that  the  entire 
heart  may  be  encased  in  fat,  and  adipose  deposit  may 
penetrate  between  the  muscular   fibres.     When  such  is  the 


FATTY  INFILTRATION  OF  THE  MYOCARDIUM.         343 

case,  the  heart  will  be  hampered  in  its  action,  and  a  further 
source  of  embarrassment  will  be  present  in  fatty  deposit 
on  the  surface  of  the  diaphragm  and  in  the  omentum. 

Fatty  Infiltration. — In  fatty  infiltration  there  is  a  deposit 
of  fat  between  the  muscle  fibres,  which  may  be  traced,  on 
careful  examination,  as  a  down-growth  from  the  overlying 
layer  of  fat  around  the  heart.  There  is  no  deposit  of  fatty 
material  in  the  muscular  fibres  themselves,  as  is  the  case 
in  fatty  degeneration.  It  is  possible  that  compression  of 
muscle  fibres  by  intervening  fat  may  lead  to  atrophy  of 
some  of  them,  and  it  is  of  course  possible  that  there  may 
be  fatty  degeneration  as  well  as  fatty  infiltration,  but  the 
two  are  quite  distinct  processes,  and  are  due  to  different 
causes. 

Distressing  shortness  of  breath  may  be  produced  by 
such  fatty  deposit  and  infiltration,  and  not  uncommonly 
there  is  a  certain  degree  of  oedema  about  the  ankles  and 
along  the  tibiae  at  night,  especially  in  hot  or  relaxing 
weather.  Such  patients  are  especially  liable  to  succumb 
to  acute  infections  such  as  pneumonia,  typhoid  fever,  etc., 
and  usually  take  anaesthetics  badly.  The  condition,  how- 
ever, is  not  attended  with  the  same  danger  as  actual 
degeneration  of  the  muscular  fibres  or  with  the  charac- 
teristic symptoms. 

Fatty  Degeneration:  Morbid  Anatomy. — Virchow  taught 
that  in  the  liver  the  presence  of  fat  in  the  cells  might  be 
merely  the  result  of  physiological  infiltration,  but  that  in 
the  heart  the  appearance  of  fatty  globules  in  the  muscle 
fibres  was  invariably  due  to  a  retrogressive  change  in  which 
there  was  actual  conversion  of  the  degenerated  protoplasm 
into  fat.     Hence  the  term  "  fatty  degeneration." 

In  1901  Eosenfeld  *  carried  out  a  series  of  experiments 
on  animals,  tending  to  show  that  in  the  heart,  as  in  the 
liver,  the  fat  found  in  the   interior  of  the  muscle  fibres  is 

*  Gent,  fur  Inn.  Med,  1901,  p.  145. 


344  HEART  DISEASE. 

really  an  infiltration,  and  is  not  formed  from  the  degene- 
rated protoplasm,  but  brought  from  fat  stores  elsewhere 
in  the  body  and  deposited  in  the  damaged  muscle. 

The  presence  of  fat  in  the  cardiac  muscle  fibres,  how- 
ever, even  though  it  be  due  to  infiltration,  and  not  a 
degeneration  in  Virchow's  sense  of  the  term,  is  pathological, 
the  result  of  a  retrogressive  morbid  change,  and,  to  avoid 
confusion,  the  term  "fatty  degeneration"  will  here  be 
retained  to  denote  this  condition. 

In  advanced  fatty  degeneration  the  heart  substance  will 
be  pale  and  softer  than  normal,  so  that  the  finger  can  be 
readily  thrust  into  it;  the  musculi  papillares  will  usually 
have  a  streaky  appearance,  the  so-called  "  tabby-cat "  stria- 
tion,  due  to  pale  strands  of  fattily  degenerated  muscular 
substance,  being  interspersed  among  healthy  fibres. 

Microscopically,  on  staining  with  osmic  acid,  it  will 
be  seen  that  the  deposits  of  fat  are  in  the  muscle  fibres 
themselves,  and  not  between  them.  The  tiny  globules  of 
fat  first  make  their  appearance  at  the  poles  of  the  muscle 
nuclei,  but  eventually  the  degenerative  process  extends 
throughout  the  muscle  fibre,  so  that  it  loses  its  striated 
appearance,  and  is  seen  to  be  filled  with  globules  of  fat. 

When  unstained,  the  granular  appearance  of  the 
degenerated  fibres  might  be  mistaken  for  the  condition 
of  "  cloudy  swelling "  or  albuminoid  degeneration  ;  but 
the  distinction  is  readily  made  by  treating  the  section 
with  acetic  acid,  which  does  not  affect  fat  globules,  but 
dissolves  the  albuminoid  granules,  or  by  staining  with 
osmic  acid,  which  gives  quite  characteristic  appearances. 

Etiology. 

1.  Sclerosis  of  the  coronary  arteries  or  obstruction  of 
these  vessels  by  endarteritis  is  one  of  the  most  important 
causes  of  fatty  degeneration.      The  heart — perpetually  at 


FATTY  DEGENERATION.  345 

work —  cannot  afford  to  be  mulcted  of  its  full  supply  of  blood. 
When,  from  any  cause,  this  is  defective,  the  wear  and  tear 
of  the  muscular  fibres,  which  must  go  on,  is  not  repaired, 
and  their  structure  breaks  down.  Whether  the  fatty 
granules  and  globules  which  are  found  within  the  sarco- 
lemma  are  deposited  there,  or  are  derived  from  the  atro- 
phied sarcous  elements,  is  not  a  matter  of  great  consequence. 
The  important  point  is  that  the  primary  change  is  atrophy 
of  the  muscle  substance,  the  invasion  of  the  fibres  by  fatty 
matter  being  secondary  to  this  and  consequent  upon  it. 

Disease  of  the  coronary  arteries,  being  thus  a  cause  of 
fatty  degeneration  of  the  heart,  the  existence  of  conditions 
which  may  lead  to  the  implication  of  the  coronary  arteries 
or  their  orifices  in  morbid  processes,  will  warrant  a  suspicion 
that  any  cardiac  weakness  which  may  be  recognized  is  the 
result  of  degeneration.  For  example,  an  aortic  murmur 
coming  on  after  middle  age  may  not  indicate  serious 
valvular  lesion,  but,  as  it  is  probably  the  result  of  athero- 
matous changes  in  the  valves  or  arterial  walls  in  close 
proximity  to  the  orifices  of  the  coronary  arteries,  there  is 
reason  to  apprehend  that  the  disease  may  cause  obstruction 
here  or  may  have  extended  to  the  vessels  themselves,  and 
progressive  weakness  of  the  heart,  were  this  to  supervene, 
would  be  attributable  to  degenerative  change  in  its  walls. 

Acute  aortitis,  again,  may  in  the  same  way  give  rise  to 
blocking  of  the  mouths  of  the  coronary  arteries.  A  like 
apprehension  attaches  to  syphilitic  disease  of  the  aorta 
and  its  valves,  which  is  not  uncommon  in  early  middle 
life,  and  especially  to  endarteritis  obliterans  affecting  the 
coronary  arteries. 

2.  Apart  from  disease  of  the  coronary  arteries,  there  is 
a  large  and  varied  group  of  causes  which  may  give  rise  to 
fatty  degeneration  of  the  heart,  comprising — - 

(a)  Certain  poisons :  phosphorus,  arsenic,  and  phlorizin. 

(b)  Acute  yellow  atrophy  of  the  liver. 


346  HEART  DISEASE. 

(c)  Acute  or  prolonged  toxaemia  of  bacterial  origin,  e.g. 
typhoid  fever,  diphtheria,  erysipelas,  pneumonia,  and  long- 
continued  suppuration. 

True  fatty  degeneration  is  by  no  means  always  present 
in  these  affections,  and  the  morbid  change  commonly  found 
is  limited  to  so-called  "  cloudy  swelling,"  or  albuminoid 
degeneration. 

(d)  Carcinoma,  phthisis,  diabetes,  and  pernicious  anremia. 
Fatty  change  in  the  heart  may  thus  be  due  to  toxins 

present  in  the  blood,  either  ingested  or  of  bacterial  origin, 
or  to  deterioration  in  the  quality  of  the  blood  from  morbid 
processes  elsewhere  in  the  body.  Consequently,  the  clinical 
features  in  this  group,  apart  from  the  signs  of  increasing 
cardiac  asthenia,  do  not  specially  point  to  the  heart  as  the 
seat  of  disease,  but  are  those  of  the  primary  affection. 

It  is  otherwise  with  the  more  serious  form  of  fatty 
degeneration  associated  with  disease  of  the  coronary  arteries, 
in  which  anginoid  attacks  and  sudden  death  from  syncope 
are  liable  to  occur. 

It  is  a  disputed  point  whether  the  sclerosis  and  narrow- 
ing of  the  coronary  vessels  or  the  fatty  change  in  the 
muscle  fibres  is  immediately  responsible  for  the  sudden 
cardiac  failure  in  these  cases. 

Huchard  *  attributes  the  symptoms  in  angina  pectoris 
entirely  to  the  coronary  sclerosis.  Gibson  f  and  Douglas 
Powell  J  admit  the  importance  of  fatty  degeneration  as  a 
possible  cause  of  angina  and  sudden  syncope.  Pratt,  §  in  a 
recent  paper  on  the  causes  of  cardiac  insufficiency,  con- 
cludes with  the  somewhat  sweeping  statement  "that  there 
is  no  evidence  to  show  that  fatty  metamorphosis  of  the 
heart  produces  cardiac  insufficiency,"  adding,  "  that  in  the 
light  of  our  present  knowledge,  anatomical  considerations, 

*  "  Maladies  du  Cceur,"  vol.  ii.  p.  1. 
t  "  Diseases  of  the  Heart  and  Aorta,"  p.  7G;-). 
J  Alllmtt's  "  System  of  Medicine,"  vol.  v.  p.  891. 
§  Bull.     "John  Hopkins  Hospital,"  vol.  xv.  p.  16?. 


FATTY  DEGENERATION.  347 

especially  coronary  sclerosis  and  interstitial  myocarditis, 
must  be  regarded  as  the  most  common  causes  of  heart  failure." 

He  bases  his  conclusions  partly  on  a  series  of  pathological 
investigations  carried  out  by  himself,  and  partly  on  experi- 
ments on  animals  performed  by  Welch,  Balint,  Hasenfeld, 
and  Fenyvessy.  As  the  fatty  change  in  these  experiments 
was  induced  by  phosphorous  poisoning,  which  is  an  acute 
process  due  to  an  irritant  poison,  whereas  the  fatty  de- 
generation under  discussion  is  very  slow  in  its  onset  and 
due  to  deficient  blood  supply,  this  evidence  can  scarcely  be 
admitted.  In  spite  also  of  the  conclusions  he  draws  from 
his  own  observations,  it  is  impossible  to  accept  the  statement 
that  fatty  degeneration  cannot  be  a  cause  of  cardiac  failure. 

The  fatty  change,  even  if  it  be  an  infiltration,  as  argued 
by  Rosenfeld,  and  not  a  "  degeneration  "  in  Yirchow's  sense 
of  the  term,  is  unquestionably  a  serious  pathological  con- 
dition, and  the  fat  deposited  in  place  of  contractile  proto- 
plasm must  necessarily  impair  the  efficiency  of  the 
muscular  fibres.  That  it  is  a  serious  lesion  is  further 
demonstrated  by  the  fact  that  spontaneous  rupture  of  the 
heart  may  occur. 

It  is  not  denied  that  sclerosis  and  narrowing  of  the 
coronary  arteries  is  the  most  important  and  serious  lesion, 
inasmuch  as  the  fatty  change  is  secondary  to  and  depen- 
dent on  this ;  but  it  is  impossible  to  determine  whether 
syncopal  attacks  and  sudden  death  in  these  cases  are  due 
to  ischemia  of  the  heart  from  coronary  stenosis,  or  to  in- 
ability of  the  fat-laden,  atrophied  muscle  to  respond  to 
the  call  when  extra  work  is  thrown  upon  it.  The  latter 
is,  at  any  rate,  quite  sufficient,  and  it  can  be  recognized 
clinically.  The  former  can  only  be  inferred.  Many  of 
the  symptoms  and  physical  signs  of  fatty  degeneration 
associated  with  coronary  stenosis,  as  will  be  seen  later,  can 
scarcely  be  ascribed  directly  to  the  vascular  lesion,  but  are 
significant  of  failing  muscular  power  of  the  heart. 


34§  HEART  DISEASE. 


Symptoms. 


There  is  little  that  is  characteristic  in  the  symptoms 
unless  we  consider  angina  pectoris  to  be  such,  and  definitely 
associate  it  with  fatty  degeneration  of  the  heart.  The 
relation  between  the  two  is  undoubtedly  very  frequent  but 
is  not  constant,  and  angina  is  therefore  reserved  for  special 
and  separate  consideration. 

In  a  large  proportion  of  cases  the  subject  of  this  affec- 
tion has  had  no  ailment  which  has  led  him  to  consult  a 
medical  man  when  he  is  overtaken  by  sudden  death  during 
exertion  or  excitement,  or  after  a  full  meal.  Or,  the  excite- 
ment and  exertion  may  be  passed  through  safely  and  death 
follow  some  hours  later,  next  day  even.  Among  the  causes 
which  precipitate  a  sudden  fatal  termination,  dilatation 
of  the  stomach  is  frequent.  Digestion  is  usually  imperfect 
from  advancing  years,  or  as  a  result  of  sluggish  circulation 
due  to  the  state  of  the  heart,  and  the  tone  of  the  muscular 
coats  of  the  stomach  is  impaired,  allowing  of  passive  dis- 
tension by  the  contained  gases,  the  products  of  fermentation. 
The  upward  expansion  of  the  stomach  is  moreover  often 
facilitated  by  a  weak  and  relaxed  condition  of  the  diaphragm, 
so  that  the  upper  line  of  gastric  resonance  can  not  unfre- 
quently  be  traced  horizontally  across  from  the  root  of  the 
ensiform  cartilage  to  the  usual  situation  of  the  apex  beat 
in  the  fifth  space.  Such  a  condition  is  attended  with  im- 
mediate danger  when  there  is  degeneration  of  the  heart 
walls,  and  may  cause  sudden  death  by  pressure  on  the 
heart,  long  before  this  would  have  resulted  from  the  state 
of  the  heart  alone. 

Rupture  of  the  heart  is  one  mode  of  termination,  and 
this  may  take  place  on  very  slight  provocation.  Some- 
times the  patient  has  been  engaged  in  his  usual  avocation 
up  to  the  moment  of  its  occurrence.  In  one  case  which 
came   under   my  observation,  an   old  gentleman   of  quiet 


FATTY  DEGENERATION.  349 

retired  habits,  with  nothing  beyond  the  weakness  incident 
to  age,  was  heard  to  knock  at  the  wall  against  which  his 
bed  was  placed,  and  was  found  dead,  the  bedclothes 
scarcely  being  disturbed.  A  neat  slit  was  found  in  the  left 
ventricle  near  the  apex  close  to  and  parallel  with  the  septum. 
In  another  case  in  which  very  advanced  fatty  degeneration 
of  the  heart  was  found  to  be  present  at  the  autopsy,  associated 
with  extreme  stenosis  of  the  coronary  arteries,  the  diameter 
of  which  was  less  than  a  millimetre,  spontaneous  rupture  took 
place  during  an  attack  of  biliary  colic.  There  had  been  no 
history  of  attacks  of  angina  or  any  warning  symptoms. 

The  bearing  of  such  occurrences  on  prognosis  is  direct 
and  simple.  No  doubt  in  many  cases  of  sudden  death  there 
have  been  warnings  which  the  patient  has  ignored  or  has 
not  spoken  of.  These  will  sometimes  be  acknowledged  in 
the  course  of  examination  when  they  have  not  been 
mentioned  spontaneously. 

When  the  course  of  the  disease  has  been  sufficiently 
chronic  to  permit  of  the  recognition  of  symptoms,  which 
in  my  experience  is  chiefly  when  the  degeneration  is 
secondary  to  change  in  the  coronary  arteries,  they  will 
be  such  as  are  produced  by  a  slackening  circulation,  and 
they  are  not  so  different  from  those  attending  dilatation 
as  to  permit  of  any  distinction  being  drawn  between  the 
two  conditions  in  an  early  stage,  without  physical  ex- 
amination. There  may,  perhaps,  be  greater  fluctuations  in 
dilatation,  though  even  in  degeneration  there  may  be  great 
temporary  improvement  under  care  and  treatment.  In 
advanced  stages  characteristic  differences  make  their 
appearance.  The  symptoms  of  advanced  dilatation  have 
already  been  described ;  those  attending  degeneration  are 
evidences  of  heart  failure  of  another  kind.  A  noteworthy 
point  is  that  well-marked  dropsy  is  rare,  and  probably  never 
occurs  in  uncomplicated  degeneration.  The  significance  of 
this  is  that  the  special  effect  of  the  disease  is  defective 


3So  HEART  DISEASE. 

pressure  in  the  arterial  system ;  and  it  is  to  this  are  due 
the  syncopal,  apoplectic,  and  epileptiform  attacks,  which, 
together  with  the  angina  pectoris,  are  the  most  character- 
istic later  effects  of  fatty  degeneration. 

The  syncopal  attacks  vary  greatly  in  intensity.  So  far 
as  they  have  come  under  my  observation,  they  have  been 
marked  rather  by  duration  than  intensity,  and  have  rarely 
been  so  complete  as  to  be  attended  with  absence  of  con- 
sciousness ;  they  have  usually  been  accompanied  by  pro- 
longed coldness  of  the  extremities  and  of  the  surface.  I 
have  not  met  with  instances  of  sudden  and  complete  loss 
of  consciousness  and  immediate  recovery  as  in  dilatation. 
These  fainting  attacks  are  very  significant,  and  are  often 
premonitory  of  fatal  syncope. 

The  apoplectiform  seizures  are  very  remarkable,  and  in 
the  absence  of  history  and  without  examination  they  are 
not  distinguishable  from  the  apoplectic  condition  resulting 
from  cerebral  hEemorrhage.  The  patient  is  unconscious ; 
the  respiration,  if  he  is  allowed  to  lie  flat  on  his  back,  may 
be  stertorous — though  stertor,  after  the  teaching  of  Dr. 
Bowles,  ought  to  be  eliminated  from  the  symptomatology 
of  apoplexy — and  there  may  be  hemiplegia,  but  this  will 
be  fugitive.  Cheyne-Stokes  breathing,  which  was  first  ob- 
served in  connection  with  fatty  degeneration  of  the  heart, 
has  not  been  present  in  the  few  cases  which  I  have  actually 
seen  in  the  apoplectiform  state,  while  I  have  met  with  it 
in  a  very  large  number  of  cases  of  ursemic  coma  and  in 
connection  with  serious  consequences  of  high  arterial  ten- 
sion. On  examination  of  the  pulse  and  heart,  however,  it 
will  be  clear  that  there  cannot  have  been  sufficient  pressure 
in  the  arteries  to  rupture  even  the  most  degenerate  vessel, 
and,  on  the  other  hand,  thrombosis  or  embolism  is  not  com- 
petent to  produce  unconsciousness  of  the  character  and 
duration  of  these  attacks.  According  to  my  experience, 
the  patient  is  never  quite  the  same  after  an  apoplectiform 


FATTY  DEGENERATION.  351 

attack ;   lie  is  feebler  in  mind  and  body,  and  sometimes 
increasingly  liable  to  syncopal  attacks. 

The  epileptiform  attacks  are  not  often  violent,  but  re- 
semble petit  mat  rather  than  a  typical  epileptic  fit ;  while, 
however,  the  convulsion  may  not  be  so  severe,  there  is 
profound  unconsciousness — not  like  epileptic  coma,  but  of 
a  syncopal  character — and  the  pulse  may  be  extremely  in- 
frequent, sometimes  less  than  twenty  in  the  minute.  In 
my  judgment,  the  heart  failure  manifested  by  the  slow 
pulse  and  the  consequent  arrest  of  the  cerebral  circulation 
are  the  cause  of  the  fits,  and  it  is  not  the  epileptiform 
attack  that  affects  the  action  of  the  heart. 

By  the  time  any  of  these  forms  of  attack  occur  the 
diagnosis  of  fatty  heart  is  usually  sufficiently  clear ;  but 
Avhen  they  are  associated  with  a  very  slow  pulse,  in  which 
the  strength  and  volume  of  the  pulse  and  the  degree  of 
impulse  of  which  the  heart  is  capable  preclude  the  idea 
of  fatty  degeneration,  they  are  probably  to  be  referred 
to  the  condition  of  Bradycardia  known  as  Stokes-Adams 
disease,  which  is  discussed  in  a  later  chapter. 

An  important  question  is  whether  there  is  anything 
characteristic  in  the  appearance  of  a  patient  suffering  from 
fatty  degeneration  of  the  heart?  A  greasy  state  of  the 
skin  with  a  sallow  pallor  of  the  face  has  been  described, 
and  if  such  a  condition  has  supervened  upon  a  previously 
healthy  complexion  the  change  would  have  significance, 
but  nothing  of  the  kind  is  present  in  a  large  majority  of 
the  cases.  Many  of  the  subjects  of  the  disease  retain  the 
look  of  health  for  a  long  time,  and  even  up  to  the  moment 
when  the  heart  ceases  to  beat.  The  degeneration  may  be 
due  to  a  local  cause — obstruction  of  the  coronary  arteries ; 
and,  even  if  a  tendency  to  general  deterioration  of  the 
tissues  is  present,  the  change  mostly  advances  so  much 
more  rapidly  in  the  heart  than  elsewhere,  that  there  is  no 
time  for  it  to  become  conspicuous  in  the  skin.     The  picture 


352  HEART  DISEASE. 

appears  to  have  been  drawn  from  cases  of  a  universal 
chronic  degeneration  of  vessels  and  heart.  The  arcus 
senilis  again,  which  has  been  said  to  indicate  the  existence 
of  cardio-vascular  degeneration,  has  no  such  significance. 

Physical  Signs. 

The  Pulse. — The  most  constant  and  significant  feature 
of  the  pulse  is  that  it  is  short  and  unsustained.  The  size 
of  the  artery  at  the  wrist  and  the  condition  of  its  walls 
may  vary  greatly.  When  the  arterial  coats  are  healthy 
they  are  apt  to  feel  extremely  thin.  The  pulse  rate  may 
be  regular  and  about  normal,  or  extremely  irregular  both 
in  force  and  time,  and  it  may  be  frecpient  or  slow.  A  very 
slow  pulse  with  extreme  low  tension  is  most  characteristic, 
but  then  it  is  the  most  rare. 

The  Heart. — The  physical  signs  may  be  described  as 
negative.  Unless  degeneration  has  attacked  a  heart  already 
enlarged  the  size  will  be  normal.  If  the  fatty  change  is 
at  all  advanced,  impulse  can  neither  be  seen  nor  felt,  or, 
if  perceptible,  it  is  only  as  a  faint  vibration.  A  heart  in 
this  condition  is  incapable  either  of  giving  a  distinct 
push  or  of  maintaining  continuous  pressure  in  the  arteries. 
The  sounds  are  weak,  sometimes  so  weak  as  to  be  almost 
inaudible ;  but  except  that  the  first  is  short,  there  is 
nothing  abnormal  about  them ;  the  intervals,  again,  are 
usually  normal.  The  very  absence  of  physical  signs,  such 
as  murmur,  or  conspicuous  modification  of  the  sounds  or 
intervals,  or  disturbance  of  the  relation  between  the  two 
sides  of  the  heart,  or  increase  of  dimensions,  when  symptoms 
of  serious  slackening  of  the  circulation  are  present,  and 
especially  when  there  have  been  anginal,  or  syncopal,  or 
apoplectic  attacks,  adds  gravity  to  the  case. 

But  a  weak,  short,  unsustained  pulse  is  common  as  a  con- 
stitutional peculiarity,  or  may  at  any  period  of  life  be  simply 


FATTY  DEGENERATION.  353 

a  result  of  general  debility,  and  impulse  and  apex  beat  may 
be  entirely  absent,  and  the  sounds  may  be  short  and  weak. 
In  young  people  there  is  no  danger  of  such  weakness  being 
taken  to  be  indicative  of  degeneration  of  the  heart,  but  it 
may  arouse  anxiety  after  middle  age,  especially  if  there  is 
also  irregularity  in  its  action. 

It  is  important  to  be  able  to  distinguish  between  func- 
tional weakness  of  this  kind  and  weakness  arising  from 
organic  disease.  Usually  this  is  accomplished  by  making 
the  patient  walk  briskly.  A  few  steps  will  often  be  suffi- 
cient. If  the  heart  is.  sound  it  rises  to  the  occasion.  The 
pulse,  and  beat,  and  sounds  are  all  more  distinct,  and  strong, 
and  regular,  whereas  the  fatty  heart  "  goes  to  pieces,"  and 
the  pulse  becomes  irregular  and  shorter  than  ever,  or  may 
even  disappear. 

Until  the  disease  is  far  advanced  the  diagnosis  of  fatty 
degeneration  of  the  heart  is  not  easy,  and  is  scarcely  to  be 
made  without  more  than  one  opportunity  of  examination. 

Prognosis. 

When  the  diagnosis  has  once  been  made,  the  prognosis, 
for  the  most  part,  can  contemplate  only  one  result ;  a  fatal 
termination  is  merely  a  question  of  time  and  circumstance. 
Excluding  cases  in  which  death  has  been  sudden  without 
warning,  the  shortest  period  in  my  experience  over  which 
characteristic  symptoms  have  extended,  together  with  recog- 
nized physical  signs,  has  been  about  six  weeks  ;  several 
patients  have  survived  the  diagnosis  two  years  before  justify- 
ing it  by  dying  suddenly.  But  circumstance  as  well  as  time 
enters  into  the  question ;  a  slight  effort,  or  a  fall,  a  little 
hurry  or  excitement,  too  hearty  a  meal,  an  attack  of  flatulent 
indigestion  or  constipation,  a  chill,  may  hurry  on  the  fatal 
termination  ;  and  on  the  other  hand,  judicious  care  may  post- 
pone it  till  the  heart  is  completely  worn  out  and  conies  to  a 

2  A 


354  HEART  DISEASE. 

standstill,  or  senile  gangrene  may  result  from  the  combined 
effects  of  cardiac  and  arterial  degeneration. 

The  question  must  be  asked,  Is  fatty  degeneration  of  the 
heart  ever  cured  or  arrested  ?  If  the  fatty  change  which 
may  result  from  typhoid  fever  and  other  toxgemias  is  to  be 
included  under  the  term,  the  answer  must  undoubtedly  be 
Yes.  The  heart  may  ultimately  regain  structural  soundness 
and  functional  vigour  when  during  the  fever  the  first  sound 
has  been  completely  lost  and  the  impulse  has  been  scarcely 
perceptible  ;  and  when  degeneration  has  been  the  result  of 
other  forms  of  blood  poisoning  or  deterioration,  it  ought  to 
be  possible,  and  now  and  then  to  occur,  that  recovery  of  the 
heart  should  follow  a  return  to  a  healthy  state  of  the  blood. 

Twelve  years  before  his  death  I  came  to  the  conclusion 
that  a  gentleman,  aged  at  the  time  about  55,  was  suffering 
from  fatty  degeneration  of  the  heart.  Spare  in  habit, 
strictly  moderate  in  eating  and  drinking,  regular  in  taking 
exercise,  and  a  great  pedestrian,  he  rapidly  lost  strength 
without  recognizable  cause,  became  breathless  on  very  slight 
exertion,  so  that  he  could  scarcely  walk  slowly  a  hundred 
yards  without  actually  stopping,  either  to  get  his  breath,  or 
on  account  of  anginoid  pain.  On  one  occasion  at  least,  while 
sitting  in  his  chair  he  became  suddenly  pale  and  uncon- 
scious, his  head  fell  on  his  chest,  and  the  jaw  dropped. 
With  this  change  in  his  health,  the  pulse  and  heart  were 
extremely  weak.  He  would  never  relinquish  exercise,  but 
continued  to  walk,  however  slowly  and  at  whatever  cost  of 
pain  and  distress,  every  day,  exercising  great  self-command 
and  measuring  his  strength  very  exactly.  Little  by  little 
he  gained  ground,  and  attained  fair  health,  but  was  capable 
of  very  little  in  the  way  of  work,  though  never  at  any  time 
were  his  intellectual  faculties  at  all  affected.  Eventually 
he  died  suddenly  in  bed. 

This  case  may  have  been  an  instance  of  arrest  and  partial 
recovery,  but  unfortunately  no  autopsy  was  obtainable. 


fatty  degeneration.  355 

Tkeatment. 

It  must  be  acknowledged  at  the  outset  that  it  is  not  in 
our  power  to  modify  in  the  least  degree  the  condition  of  the 
cardiac  muscular  fibre  when  far  advanced  in  fatty  degenera- 
tion, and  that  we  can  do  very  little,  if  anything,  to  arrest  the 
progress  of  the  deterioration  when  it  has  reached  a  stage  at 
which  it  is  recognizable  either  through  symptoms  or  by 
physical  signs.  Even  at  a  very  early  period  we  should 
doubt  the  possibility  of  reversing  a  process  which  in  some 
cases  is  an  inherited  tendency  to  natural  decay  at  a  given 
time  of  life,  in  others  an  effect  of  imperfect  blood  supply 
due  to  narrowing  of  the  coronary  arteries. 

If,  indeed,  the  degeneration  has  been  the  result  of  acute 
disease,  such  as  typhoid  fever,  time  and  care  will  bring  about 
a  restoration  of  the  muscular  fibres  ;  but  this  is  not  fatty 
degeneration  of  the  same  nature  as  that  due  to  coronary 
sclerosis,  but  is  rather  a  secondary  consequence  of  the 
condition  of  so-called  cloudy  swelling,  which  is  a  result  of 
prolonged  toxaemia. 

When,  again,  the  condition  is  not  true  degeneration  of 
the  muscular  fibres,  but  a  fatty  heart,  due  to  a  sedentary 
life,  with  privation  of  fresh  air  and  neglect  of  exercise, 
together  with  undue  indulgence  in  alcoholic  drinks  and  in 
the  pleasures  of  the  table,  there  is  not  then,  at  any  rate 
till  an  advanced  stage,  true  fatty  degeneration,  but  a  deposit 
of  fat  between  the  muscular  fibres  or  fatty  infiltration.  In 
such  cases  careful  dieting  and  graduated  exercise,  such  as 
the  CErtel  treatment,  may  reverse  the  degenerative  tendency 
and  even  cause  a  gradual  absorption  of  the  fatty  tissue 
already  deposited  in  and  around  the  heart  as  well  as 
elsewhere. 

While,  however,  acknowledging  the  limitation  of  thera- 
peutics in  dealing  with  the  organic  change,  we  are  not  alto- 
gether powerless  to  avert  its  consequences,  and  by  so  doing 


356  HEART  DISEASE. 

to  prolong  life.  We  see  from  time  to  time,  on  post-mortem 
examination,  the  heart  so  far  gone  in  fatty  change  that  it  is 
scarcely  recognizable  as  muscle,  either  to  the  naked  eye  or 
under  the  microscope.  Such  change  must  have  been  long 
in  progress,  and  the  subject  of  it  must  have  lived  for 
months  if  not  for  years,  while  the  slightest  obstruction  in 
either  pulmonary  or  systemic  circulation  would  have  brought 
the  heart  to  a  standstill,  and  a  shock,  a  fall,  or  an  indi- 
gestible meal,  would  have  been  fatal.  We  meet  with  cases 
of  this  kind  during  life,  in  which  the  decay  of  the  mental 
and  bodily  powers  is  so  slow  as  to  be  almost  imperceptible, 
or  in  which  thrombosis  of  one  cerebral  vessel  after  another 
brings  the  patient  to  a  state  of  dementia  or  bed-ridden 
paralysis  from  general  or  local  cerebral  softening.  Or 
the  immediate  cause  of  death  may  be  senile  gangrene.  It 
is  not  that  results  such  as  those  just  named  are  desirable — 
death  would  be  preferable  were  we  allowed  to  choose — but 
cases  of  the  kind  serve,  with  others,  to  show  that  prolonga- 
tion of  life  is  possible  when  the  central  organ  of  the 
circulation  can  barely  keep  the  blood  in  motion,  and  to 
illustrate  the  conditions  under  which  this  is  observed. 
These  conditions  are  a  gradual  diminution  of  mental  and 
bodily  activity,  together  with  attention  to  diet  and  regula- 
tion of  the  bowels.  The  setting  in  of  softening  of  the  brain, 
or  an  attack  of  paralysis,  not  unfrequently  seems  to  put  an 
end  to  cardiac  symptoms  and  to  prolong  life ;  the  sufferer  is 
no  longer  his  own  master ;  he  cannot  undertake  business  or 
go  about,  his  food  is  under  orders,  and  the  action  of  the 
bowels  is  known  to  others  besides  himself. 

If,  in  an  early  stage  of  fatty  degeneration  of  the  heart, 
the  same  command  over  the  patient's  mode  of  life  and  the 
same  knowledge  of  the  -state  of  his  secretions  were  attain- 
able, not  only  might  life  be  made  longer  by  many  years, 
but  much  suffering  Avhich  is  seen  to  arise  out  of  this  form 
of  disease    might    be  averted.      It  is  unnecessary,  and    it 


FATTY  DEGENERATION.  357 

would  be  impossible  to  enter  into  particulars  with  regard  to 
trie  amount  of  work  and  exercise  to  be  permitted,  or  trie 
quantity  and  kind  of  food  to  be  allowed  ;  the  latter  may, 
and  indeed  in  most  cases  must,  be  liberal  and  varied,  but 
precautions  must  be  taken  against  an  inordinate  appetite, 
and  it  is  always  safest  to  let  some  judicious  relative  or 
attendant  who  knows  his  likings  and  what  suits  him,  help 
the  patient  at  meals,  and  decide  for  him  what  dishes  and 
what  quantity  will  be  good  for  him,  acting  under  the  advice 
of  the  medical  man. 

Proper  regulation  of  the  bowels  is  of  the  utmost  import- 
ance. As  years  increase  people  are  apt  to  become  less 
observant,  and  to  take  it  for  granted  that,  so  long  as  the 
habitual  regularity  in  going  to  stool  obtains,  the  action  of 
the  bowels  is  satisfactory  and  efficient,  whereas  it  may  be 
that  the  evacuation  is  much  too  small  in  amount.  Accumu- 
lation thus  gradually  takes  place,  and  it  is  not  uncommon 
for  a  second  daily  call  to  relieve  the  bowels,  resulting  from 
this,  to  be  regarded  as  evidence  of  improvement  in  their 
action.  The  statements  of  patients,  then,  with  regard  to 
this  function,  are  not  always  trustworthy,  and  the  testimony 
of  a  competent  observer,  or  inspection  by  the  medical  man, 
is  necessary.  The  quantity  of  fsecal  matters  which  may 
unconsciously  accumulate  in  the  colon  is  astonishing,  and 
the  prevention  of  such  an  occurrence  is  essential  to  the 
well-doing  of  a  patient  whose  heart  is  organically  weak. 
For  the  regulation  of  the  bowels  mild  aloetic  aperients  are 
best,  with  pil  hydrarg.  and  colocynth  occasionally  in  small 
doses,  if  there  is  arterial  tension.  Any  tendency  to  flatulent 
distension  of  the  stomach  must  be  counteracted,  as  far  as 
possible,  by  careful  dieting  and  the  administration  of  alkalies 
and  carminatives.  Bitter  tonics  may  be  given,  and  massage 
or  gentle  exercise  is  often  of  great  service.  Extremes  of 
heat  and  cold  should  be  avoided,  and  a  dry,  bracing,  healthy 
spot  in  the  country  should  be  selected  as  a  residence. 


358  HEART  DISEASE. 

Aneurysm  of  the  heart  is  of  rare  occurrence,  and  seldom 
gives  rise  to  any  physical  signs  or  symptoms  by  which  it 
can  be  diagnosed  during  life.  It  usually  affects  the  left 
ventricle.  It  results  from  local  destruction  or  weakening 
of  a  portion  of  the  heart  wall,  which  may  be  due  to  break- 
ing down  of  a  gumma,  abscess  from  a  septic  embolus, 
softening  from  thrombosis,  or  embolism  of  a  branch  of  the 
coronary  artery. 

It  is  usually  lined  by  laminated  clot,  and  varies  in  size. 
In  one  instance  I  have  seen,  the  aneurysm  was  situated  in 
the  lower  half  of  the  wall  of  the  left  ventricle,  and  was 
three  inches  in  diameter.  It  was  completely  filled  up  with 
layers  of  laminated  clot.  It  gave  rise  to  no  distinctive 
physical  signs  or  symptoms  during  life,  and  did  not  appear 
to  be  the  immediate  cause  of  death. 

New  growths  of  the  heart  are  rarely,  if  ever,  primary. 
Secondary  growths  are  also  very  uncommon ;  but  nodules  of 
sarcomatous  or  carcinomatous  growths  in  the  heart  wall  are 
occasionally  met  with  secondary  to  growths  in  other  organs. 


CHAPTER  XXV. 
ANGINA   PECTORIS. 

CHARACTERISTICS  OP  TRUE  ANGINA — ASSOCIATED  SYMPTOMS 
—  EXCITING  CAUSES  OP  PAROXYSMS— ETIOLOGY  AND 
MORBID  ANATOMY — DISCUSSION  OP  THEORIES  ADVANCED 
TO  EXPLAIN  THE  PAIN  —  DIAGNOSIS  —  PROGNOSIS — 
TREATMENT. 

While  heart  disease  generally  is  remarkable  for  the  almost 
entire  freedom  from  pain — so  that  when  patients  come 
complaining  of  pain  in  the  cardiac  region,  it  is  a  presumption 
against  the  existence  of  any  serious  organic  lesion  rather 
than  an  indication  of  any  such  change — there  is  one  form 
of  pain  in  and  around  the  heart,  angina  pectoris,  which  is 
very  definite  and  constant  in  its  significance  of  disease  and 
danger.  The  term  "  angina  pectoris,"  or  pain  in  the  chest, 
has  come  to  have  a  specialized  meaning,  and  is  commonly 
employed  to  denote  a  complex  group  of  symptoms  associated 
with  certain  grave  pathological  changes  in  the  heart  and 
coronary  arteries. 

As  an  account  of  the  distinctive  features  of  "angina 
pectoris  "  involves  a  discussion  of  the  associated  symptoms, 
it  will  be  more  convenient  to  describe  these  first,  and  to 
defer  the  consideration  of  the  etiology  and  morbid  anatomy 
to  a  later  period. 

Characteristics  op  true  Angina  Pectoris  :  Associated 

Symptoms. 

In  a  typical  attack  of  angina  there  is  intense  pain  in 
some  part  of  the  cardiac  region,  most  frequently  behind  the 


360  HEART  DISEASE. 

sternum,  with  radiation  down  the  left  arm,  but  occasionally 
across  the  upper  part  of  the  chest,  in  the  left  breast,  or  in 
the  neighbourhood  of  the  ensiform  cartilage.  Accompany- 
ing the  pain  is  a  sense  of  utter  helplessness  and  extreme 
fear  and  dread.  The  patient  keeps  still,  not  daring  to 
moye,  and  feels  as  if  he  were  in  the  act  of  dying.  He  will 
say  afterwards  that  if  the  pain  had  lasted  another  moment 
he  must  have  died.  In  no  other  condition  is  the  physical 
agony  of  dying  realized  in  the  same  degree.  The  two 
elements  of  pain  and  sense  of  impending  death  coexist 
in  a  true  paroxysm  of  angina,  and  are  almost  equally 
characteristic. 

The  pain  differs  in  character  and  situation  and  in  in- 
tensity in  different  cases.  Some  sufferers  will  say  it  is 
indescribable — nothing  in  their  previous  experience  suggests 
even  a  comparison ;  others  speak  of  the  pain  as  severe 
cramp  in  the  heart,  or  as  if  the  heart  were  gripped  by  an 
iron  claw ;  while  pain  of  a  shooting,  neuralgic  character 
sometimes  intermittent,  sometimes  persistent,  seems  to 
radiate  from  the  chest  to  the  left  shoulder,  down  the  inner 
side  of  the  arm  to  the  forearm,  and  the  ring  and  little  fingers. 
Occasionally  there  is  a  sensation  as  of  the  wrist  being 
grasped  so  tightly  as  to  cause  pain.  With  the  pain  in  the 
heart  there  may  be  pain  down  both  arms  or  shooting  up  into 
the  left  side  of  the  neck,  very  rarely  in  the  right  arm  only. 
Occasionally  the  pain  may  be  felt  first  in  the  wrist  or  arm 
and  seem  to  travel  up  to  the  chest,  or  may  come  in  the  inner 
side  of  the  arm  as  a  kind  of  warning  of  an  attack.  Another 
description  of  the  pain  is  that  it  feels  as  if  the  sternum  were 
being  crushed  back  to  the  spine,  or,  again,  as  if  the  whole 
chest  were  being  held  in  a  vice.  In  other  cases  the  pain  is 
compared  to  a  bar  of  iron  across  the  upper  part  of  the  chest ; 
in  others,  again,  to  a  ton  weight  upon  the  lower  part  of  the 
chest.  The  ramifications  of  the  cardiac  plexus  and  its  com- 
munications witli  other  nerves  make  the  radiation  of  pain 


ANGINA   PECTORIS.  361 

in  all  the  various  directions  enumerated  comprehensible, 
and  the  nerve  of  Wrisberg  has  been  specially  instanced  as 
explaining  the  pain  in  the  left  arm,  but  no  explanation  can 
be  given  why  in  one  case  the  pain  is  felt  in  one  part  of  the 
cardiac  region,  and  has  some  particular  character,  and  takes 
a  given  direction  down  one  arm  or  both  or  through  to  the 
back,  while  in  another  case  the  seat,  character,  and  exten- 
sion of  the  pain  are  quite  different.  It  is  not  a  pressure 
effect  on  the  plexus  outside  the  heart,  neither  heart  nor 
aorta  being  necessarily  enlarged,  and  fusiform  dilatation  of 
the  arch  of  the  aorta  is  common  without  anginoid  pain  ; 
there  can  be  no  stretching  or  mechanical  irritation  of  the 
nerve-ramifications  beneath  the  endocardium  at  all  com- 
parable to  that  which  takes  place  in  acute  dilatation  of  the 
heart.  It  seems  to  me  that  the  pain  is  a  danger  signal 
given  by  the  sensory  nerves  of  the  heart.  The  radiation 
of  irritation  giving  rise  to  its  extension  takes  place  in 
the  spinal  cord,  as  will  be  shown  in  the  next  chapter. 

An  interesting  point  is  that  at  the  end  of  a  paroxysm 
there  is  usually  flatulent  eructation  from  the  stomach. 
The  attacks  are  therefore  very  commonly  attributed  to 
flatulence,  and  distension  of  the  stomach  by  food  or  gases 
may  undoubtedly  be,  and  often  actually  is,  an  exciting 
cause,  but  more  frequently  the  sensation  as  of  wind  on  the 
stomach  is  only  a  part  of  the  general  commotion,  and  is  due 
to  communicated  or  sympathetic  irritation  of  the  gastric 
distribution  of  the  vagus,  the  cardiac  branches  of  which  are 
primarily  implicated.  The  escape  of  gas  from  the  stomach 
is  often  a  signal  that  the  paroxysm  is  over  rather  than  the 
means  of  bringing  it  to  an  end.  Occasionally  there  is  a 
vehement  desire  to  pass  urine,  although  the  bladder  may 
at  the  time  be  empty. 

The  duration  of  the  attacks  is  very  varied ;  sometimes 
it  can  be  reckoned  in  seconds.  Most  frequently,  perhaps,  a 
paroxysm    will  last  a   few  minutes,  but  I   have   known  a 


362  HEART  DISEASE. 

patient  sit  in  the  same  position  almost  through  an  entire 
night,  not  venturing  to  make  the  slightest  movement  and 
scarcely  seeming  to  breathe,  while  the  perspiration  rolled 
off  his  forehead  and  came  through  his  clothes.  According 
to  my  experience,  it  is  when  the  attack  comes  on  in  the 
night,  without  provocation  by  exertion  or  exposure,  that  it  is 
protracted.  When  it  is  started  by  exertion  it  generally 
ceases  soon  after  the  exertion  is  left  off. 

While  it  would  not  be  justifiable  to  say  that  a  patient 
was  the  subject  of  angina  pectoris  unless  he  had  had  one  or 
more  paroxysms  of  intense  radiating  pain,  associated  with 
a  sense  of  immediately  impending  death,  it  must  be  ad- 
mitted that  attacks  of  true  angina  occur  which  fall  short 
of  the  typical  development.  For  example,  when  a  patient 
has  been  taught  prudence  by  one  or  more  bad  attacks,  he 
may,  by  standing  still  on  the  first  warning,  or  by  taking 
remedies,  cut  short  the  paroxysm,  which  will  then  have 
been  represented  only  by  the  initial  pain  in  the  breast  or 
arm  without  the  mortal  dread.  It  is  possible,  therefore, 
that  before  any  characteristic  attack  has  occurred,  pains  of 
a  similar  kind  and  intensity,  disregarded  by  the  patient  or 
relieved  by  rubbing  the  chest  or  arm,  may  have  the  same 
significance  as  a  fully  developed  paroxysm. 

Again,  a  patient  who  has  had  attacks  of  true  angina 
may  cease  to  suffer  pain,  but  may  have  attacks  of  what  he 
calls  faintness,  in  one  of  which  he  ultimately  dies.  These, 
which  have  lost  their  title  to  the  name  angina,  have  an 
equally  serious  significance.  They  are  sometimes  called 
angina  pectoris  sine  dolore. 

The  aspect  of  the  patient  is  one  of  extreme  anxiety  or 
alarm.  He  is  usually  pale  and  often  livid  round  the  mouth, 
but  it  is  said  that  sometimes  the  colour  does  not  change. 
A  cold  perspiration  usually  bursts  out  on  the  forehead,  and 
may  be  so  copious  as  to  drip  off  the  face.  The  pulse,  in  the 
rare   instances   in  which   I   have   had   the   opportunity  of 


ANGINA   PECTORIS.  363 

examining  it  during  a  paroxysm,  has  been  irregular,  small, 
and  weak.  In  some  cases  it  has  been  reported  to  be  very 
small  from  contraction  or  spasm  of  the  arteries.  In  others, 
again,  it  has  scarcely  been  affected  at  all. 

Exciting1  Causes  of  a  Paroxysm. — Great  importance  attaches 
to  the  exciting  cause  of  the  paroxysms.  In  the  first  instance 
they  are  almost  always  brought  on  by  exertion.  The  patient, 
while  walking  perhaps  more  sharply  than  usual,  or  uphill, 
or  against  a  wind,  is  more  or  less  suddenly  arrested  by  pain 
in  the  chest,  with  a  feeling  as  if  the  heart  were  about  to 
stop  and  he  to  fall  down  dead.  On  standing  still  the  pain 
gradually  passes  off,  and  he  is  able  to  resume  his  walk,  but 
only  feebly  and  gently.  For  a  while  the  attacks  only  occur 
when  provoked  by  exertion,  but  more  and  more  easily  as 
time  goes  on,  and  they  tend  to  become  more  severe.  They 
are  more  readily  induced  when  a  walk  is  taken,  or  any 
imprudent  exertion,  such  as  stooping,  drawing  on  boots, 
pulling  open  a  drawer,  pushing  up  a  window,  is  made  soon 
after  a  meal,  especially  after  breakfast.  External  cold, 
again,  predisposes  to  an  attack,  and  exercise,  which  can 
be  taken  with  impunity  in  mild  weather,  brings  on  a 
paroxysm  if  the  air  is  cold  and  damp.  Attacks,  again, 
may  be  brought  on  by  indigestion  or  constipation,  appa- 
rently either  through  reflex  disturbance  of  the  heart,  or  as 
a  result  of  pressure  from  the  distended  stomach  or  colon 
carrying  the  diaphragm  upwards  and  obstructing  mechani- 
cally the  action  of  the  heart  and  the  expansion  of  the 
lungs. 

They  are  also  liable  to  occur  during  the  night,  and  may 
be  induced  in  various  ways.  On  first  lying  down,  the 
contact  of  cold  sheets  may  have  this  effect  by  causing 
contraction  of  the  peripheral  arterioles,  and  thus  throwing 
increased  work  on  the  heart ;  the  exertion  of  undressing- 
may  predispose  to  an  attack,  or  the  upward  pressure  of  the 
abdominal  viscera,  on  assuming  the  horizontal  position,  may 


364  HEART  DISEASE. 

embarrass  trie  heart.  An  attack  may  come  on  after  sleep 
when  the  vigour  of  the  circulation  has  run  clown,  and  when 
possibly  also  evolution  of  gases  in  the  stomach,  and  disten- 
sion of  this  viscus  or  of  the  colon,  have  given  rise  to 
pressure  on  the  diaphragm. 

It  is  clear  that  the  great  exciting  cause  is  a  demand  for 
increased  effort  on  the  part  of  the  heart  to  which  it  is  not 
equal,  or  occasionally  the  cause  may  be  interference  with 
the  movements  of  the  heart  by  a  dilated  stomach  and  colon. 

Etiology  and  Morbid  Anatomy. 

The  conditions  of  the  heart  associated  with  angina 
pectoris  are  varied,  but  perhaps  the  most  remarkable  and 
significant  point  in  the  relations  between  heart  disease  and 
angina  is  that  angina  does  not  attend  the  chain  of  events 
through  which  stenosis  or  incompetence  of  the  mitral  valve 
proves  fatal,  and  is  not  among  the  symptoms  which  arise 
out  of  the  valve  lesion  and  its  effects  upon  the  heart.  This 
fact  was  duly  emphasized  by  Walshe,  in  his  classical  work 
on  the  heart,  and  no  exception  to  it  has  occurred  in  my 
experience.  I  have,  indeed,  known  instances  in  which, 
after  attacks  of  angina  had  occurred  at  intervals  for  many 
months,  mitral  regurgitation  has  supervened  with  dilatation 
of  the  left  ventricle,  and  concurrently  with  the  establish- 
ment of  so-called  mitral  symptoms — pressure  in  the  pulmo- 
nary circulation,  dilatation  of  the  right  side  of  the  heart, 
and  dropsy — the  angina  has  ceased.  In  these  particular 
circumstances  Balfour's  view,  that  the  giving  way  of  the 
mitral  valve  may  be  an  advantage  to  the  sufferer  from  aortic 
disease,  is  perhaps  justified,  or  it  is  possible  that  in  such 
cases  breathlessness  may  compel  the  cessation  from  exerti<  »n 
before  the  condition  which  gives  rise  to  pain  is  reached. 

Aortic  stenosis  may  be  attended  with  true  angina,  as 
may  also  aortic  incompetence  or  combination  of  the  two 
conditions  of  the  aortic  valve.     In  association  with  aortic 


ANGINA   PECTORIS.  365 

valvular  disease  angina  may  be  met  with  in  early  adult 
life,  and  may  continue  for  many  years  without  proving  fatal. 
The  sense  of  impending  death  is,  however,  not  so  fully  pro- 
nounced in  aortic  cases,  though  the  pain  may  be  very  severe. 

Injury  to  the  root  of  the  aorta  has  been  known  to  give 
rise  to  ano-ina.  I  have  had  a  case  under  observation  for 
several  years,  in  which  a  severe  crush  of  the  chest  gave 
rise  to  a  double  aortic  murmur  and  to  distressing  attacks 
of  angina.  For  a  time  the  attacks  came  on  very  frequently, 
even  while  the  patient  was  kept  in  bed,  and  they  continued 
to  occur  on  very  slight  provocation,  requiring  frequent 
recourse  to  nitro-glycerine,  which  the  patient  took  in  con- 
siderable quantity.  There  was  scarcely  any  compensatory 
hypertrophy  and  dilatation  in  this  patient,  and  he  was 
never  able  to  work. 

In  aortitis  affecting  the  root  of  the  aorta  there  is  usually 
angina,  the  attacks  at  first  slight,  increasing  in  intensity 
and  duration,  and  coming  on  more  frequently  as  the  disease 
advances.  The  heart  rapidly  becomes  weaker  without  notable 
enlargement,  the  impulse  more  feeble,  the  sounds  weak  and 
short.  Both  the  angina  and  the  weakness  of  the  heart  point 
to  interference  with  the  coronary  circulation,  and  the  orifices 
of  the  coronary  arteries  are  found  small  and  contracted  by 
the  swelling  of  the  walls  of  the  aorta. 

Gout. — Attacks  of  pain  in  the  region  of  the  heart  may 
occur  in  gouty  subjects.  Frequently  they  are  merely  reflex 
due  to  gastric  disturbances.  True  angina,  when  it  is  met 
with,  is  to  be  attributed  not  directly  to  the  gout,  but  to  the 
degenerative  vascular  lesions  to  which  gout  predisposes,  and 
which  may  affect  the  aorta  or  coronary  arteries. 

Bacterial  Infections. — Angina  has  followed  recovery  from 
plague  in  two  cases  I  have  seen,  and  was  experienced  on 
slight  exertion  for  several  years,  and  a  characteristic  attack 
of  angina  has  been  described  to  me  as  having  occurred  in 
intermittent  fever. 


366  HEART  DISEASE. 

Fatty  Degeneration  of  the  Heart. — In  a  very  large  pro- 
portion of  cases  in  which  angina  proves  fatal  the  heart  is 
found,  when  examined  after  death,  to  be  in  a  more  or  less 
advanced  stage  of  fatty  degeneration.  The  fatty  change  may 
be  so  far  advanced  that  the  fingers  sink  into  the  walls  of  the 
heart  on  slight  pressure,  and  scarcely  any  sound  muscular 
fibres  can  be  found  on  microscopic  examination.  Sometimes 
it  may  appear  to  be  comparatively  slight,  and  only  evident  to 
the  naked  eye  as  yellow  patches  or  strise  in  the  ventricular 
walls  and  in  the  musculi  papillaries,  but  microscopic 
examination  shows  widespread  fatty  degeneration  and  fat 
globules  in  fibres  that  appear  to  be  normal  to  the  naked 
eye.  The  heart  may  be  normal  in  size  or  perhaps  greatly 
dilated,  or  there  may  be  a  considerable  degree  of  hypertrophy. 
The  coronary  arteries  will  invariably  be  found  to  be  diseased. 
Sometimes  they  can  be  dissected  out  as  hard,  rigid,  cal- 
careous tubes  from  the  auricular  grooves,  and  frequently 
their  walls  are  so  thickened  that  the  lumen  is  almost 
obliterated. 

Fibrosis. — In  some  instances  the  morbid  condition 
found  is  fibrosis,  general  or  local,  associated  with  coronary 
sclerosis,  or  possibly  the  result  of  myocarditis. 

There  may  be  little  or  no  change  recognizable  in  the 
wails  of  the  heart,  and  the  coronaries  at  first  sight  may 
appear  to  be  healthy,  especially  when  the  first  attack  has 
proved  fatal  or  death  has  supervened  after  a  few  paroxysms. 
It  is  probable,  however,  that  in  such  cases,  on  careful 
examination,  obliteration  of  a  branch  of  the  coronary  artery 
by  endarteritis  or  its  obstruction  by  an  embolus  or  thrombus 
will  be  discovered. 

Angina  Vasomotoria. — Angina  is  also  met  with  in  a 
certain  proportion  of  cases  of  high  arterial  tension  associated 
with  general  arterio  sclerosis,  in  which  the  maintenance  of 
a  high  degree  of  pressure  in  the  circulation  precludes  the 
existence  of  any  marked  degree  of  fatty  degeneration   in 


ANGINA   PECTORIS.  367 

the  cardiac  muscle.  In  this  class  of  cases  the  paroxysms 
of  angina  appear  to  depend  on  increased  arterio-capillary 
resistance,  which  raises  the  blood  pressure  and  throws  extra 
work  on  the  heart.  To  this  group  the  term  "  angina  vaso- 
motoria "  may  be  conveniently  applied  to  distinguish  them 
from  cases  in  which  fatty  degeneration  of  the  heart  is 
pronounced,  and  inherent  cardiac  weakness  is  the  prominent 
feature.  The  heart  is  hypertrophied  and  may  be  capable  of 
powerful  contraction,  and  the  circulation  in  the  coronaries 
may  be  sufficient  for  ordinary  needs,  but  when  the  arterial 
tension  is  further  raised  by  exertion  or  increase  of  peripheral 
resistance  attacks  of  angina  are  induced.  I  have  thought 
it  well  to  make  special  allusion  to  this  form  of  angina, 
which  has  been  termed  "  vasomotoria,"  as  the  prognosis  is 
less  serious,  and  more  satisfactory  results  can  be  obtained 
from  suitable  treatment  than  in  cases  in  which  angina  is 
associated  with  fatty  degeneration  of  the  cardiac  muscle. 
The  attacks  of  angina  cannot,  of  course,  be  attributed  simply 
to  the  high  arterial  tension,  which  is  met  with  in  an 
extreme  degree,  without  angina,  in  chronic  Bright's  disease 
and  various  other  conditions.  The  real  underlying  cause 
will  be  found  to  be  partial  occlusion  of  the  mouth  of  the 
coronary  arteries  by  degenerative  changes  in  the  aorta,  or 
sclerosis  of  the  coronary  vessels,  which  are  results  of  the 
high  arterial  tension.  There  will  not,  as  a  rule,  be  extreme 
stenosis  of  the  coronary  vessels  such  as  may  be  present  in 
fatty  hearts,  but  rather  thickening  and  rigidity,  and  it  may 
be  calcification  of  their  walls,  the  loss  of  contractility,  which 
must  have  seriously  impaired  the  circulation  in  the  heart 
during  life. 

Conclusions. — It  will  be  seen  from  a  review  of  the  above- 
mentioned  etiological  factors  that  interference  with  the 
flow  of  blood  through  the  coronary  arteries  from  disease  of 
their  walls,  from  thrombosis  or  embolism,  or  from  narrowing 
of  their  orifice  by  atheromatous  changes  in  the  aorta,  is  by 


368  HEART  DISEASE. 

far  the  commonest  cause  of  true  angina  pectoris,  and  is  the 
only  constant  pathological  lesion  found  post-mortem.  In 
fatty  or  fibroid  degeneration  of  the  heart,  with  which  angina 
is  frequently  associated,  sclerosis  of  the  coronary  vessels  is 
present,  and  in  the  aortic  lesions  to  which  reference  has 
been  made  above  there  is  either  atheromatous  degeneration 
of  the  aorta,  which  may  involve  the  orifice  of  one  or  both 
coronary  arteries,  or  the  coronaries  themselves  are  diseased. 
In  cases  of  angina  following  acute  bacterial  infections,  it 
may  be  that  acute  arteritis  is  set  up  in  the  coronary 
arteries,  or  in  the  vasa  vasorum  supplying  them,  Avhich 
will  subsequently  lead  to  degenerative  changes  in  the 
coronary  vessels  from  impaired  nutrition.  Of  this,  however, 
we  have  no  direct  proof.  Huchard,*  after  a  very  compre- 
hensive enumeration  and  a  masterly  discussion  of  all  the 
possible  causes  of  angina,  sums  up  in  the  following  words, 
"  II  n'y  a  pas  plusieurs  angines  de  poitrine,  il  n'y  a 
qu'une  seule,  l'angine  coronarienne."  He  |  admits,  however, 
that  in  tobacco  poisoning  there  may  be  attacks  of  true 
angina  without  coronary  sclerosis.  These  he  attributes  to 
temporary  spasm  of  the  coronary  arteries, 

Theories  advanced  to  explain  the  Pain. 

Numerous  theories  have  been  advanced  to  explain  the 
pain  of  "  angina  pectoris." 

Stretching  of  the  Heart  Muscle  Fibres. — It  might  be 
supposed  that  mechanical  stretching  of  the  muscle  fibres 
in  the  endeavour  to  overcome  resistance  in  the  circulation 
would  give  rise  to  pain,  but  acute  dilatation  of  the  heart  may 
occur  under  various  conditions  without  giving  rise  to  angina. 

Neuralgia. — It  has  been  suggested  that  the  pain  might 

be  due  to  cardiac  neuralgia,  but  the  nature  of  the  attacks 

and  of  the  exciting  causes  which  induce  them  are  scarcely 

*  "  Maladies  du  Coeur,"  vol.  ii.  p.  13d. 
t  Ibid.,  p.  1U5. 


ANGINA   PECTORIS.  369 

compatible  with  this  theory.  Angina,  moreover,  is  far 
more  common  in  men  than  women,  whereas  the  converse  is 
the  case  with  neuralgia. 

Impairment  of  Contractility  of  the  Heart  Muscle. — Mac- 
kenzie,* in  a  paper  on  the  cause  of  angina,  gives  an 
interesting  series  of  pulse  tracings,  two  of  which,  taken 
during  an  attack  of  angina,  show  the  presence  of  the  "  pulsus 
alternans,"  that  is,  a  large  beat  regularly  alternating  with 
a  small  beat.  This  pulse  is  not  necessarily  associated  with 
angina,  but  is  frequently  met  with  in  other  conditions.  He 
regards  the  "  pulsus  alternans  "  as  evidence  of  impairment 
.  of  the  contractile  power  of  the  heart  muscle,  and  states 
that  in  cases  of  angina,  the  same  exciting  cause — extra 
strain  on  the  heart — may  provoke  both  angina  pectoris 
and  the  alternating  action  of  the  heart,  and  that  both  may 
disappear  with  removal  of  the  cause.  He  therefore  con- 
cludes that  angina  pectoris  will  be  found  to  be  associated 
with  impairment  of  the  function  of  contractility  of  the  heart. 

Spasm  of  the  Heart. — The  condition  of  the  heart  during 
the  attacks  has  been  supposed  to  be  one  of  spasm,  but  there 
are  many  objections  to  this  view,  and  ideas  as  to  what  is 
meant  by  spasm  of  the  heart  in  the  anginal  paroxysm  by 
those  who  have  employed  the  term  have  been  diverse  and 
vague.  If  by  spasm  of  the  heart  is  understood  tonic  con- 
traction or  an  unrelaxing  systole,  this  is  certainly  not  the 
condition  present.  The  heart  has  never  been  found  in  this 
state  after  death,  and  in  most  cases  is  incapable  of  such 
contraction  from  the  state  of  its  walls.  No  pulse  would  be 
possible  were  the  heart  in  a  spasm  of  this  kind,  and  the 
pulse,  though  small  and  often  irregular,  can  usually  be  felt. 
It  has,  indeed,  in  some  cases  been  apparently  unaffected  by 
the  paroxysm. 

But  by  spasm  may  be  meant  an  irregular  and  partial 
contraction  like  cramp  in  voluntary  muscles,  or  a  fibrillar 
*  B.M.J.,  vol.  ii.  1905,  p.  845. 

2    B 


37°  HEART  DISEASE. 

contraction,  such  as  is  sometimes  induced  by  faradic  cur- 
rents in  muscle  under  experiment.  The  late  Dr.  Matthews 
Duncan,  in  the  last  conversation  I  had  the  honour  to  hold 
with  him,  suggested  that  the  state  of  the  heart  in  angina 
pectoris  might  be  like  hour-glass  contraction  of  the  uterus. 
He  had  at  that  time  experienced  the  pain. 

Views  of  this  kind  cannot  be  proved  to  be  wrong,  but 
objections  might  be  raised,  and  the  central  fact  and  essen- 
tial significance  of  angina  is  that  stress  is  put  upon  the 
heart,  to  which,  for  the  moment,  it  is  unequal. 

One  of  the  main  causes  of  such  stress  is  resistance  in  the 
peripheral  circulation,  or,  in  other  words,  high  arterial 
tension,  and  we  owe  to  Lauder  Brunton  the  knowledge  that 
in  many  attacks  of  angina  there  is  an  aggravation  of 
habitual  high  tension  by  a  general  contraction  of  the  arteri- 
oles. But  the  habitual  state  of  the  arterial  circulation  may 
be  one  of  relaxed  arterioles  and  capillaries  and  low  tension, 
so  that  the  heart  has  no  abnormal  resistance  to  overcome. 
Here  sudden  general  arterial  spasm  would  put  the  heart  to 
greater  stress  than  if  the  habitual  tension  were  high,  since 
the  contrast  between  the  work  demanded  would  be  greater. 
Huchard  considers  that  the  attacks  of  anginoid  pain  are 
due  to  ischemia  of  the  heart,  either  from  spasm  of  the 
coronary  arteries,  or  from  the  relatively  deficient  blood 
supply  through  the  narrowed  vessels  when  exertion  or 
increase  of  arterial  tension  demands  increased  blood  supply 
to  the  heart.  He  compares  the  condition  of  the  heart  to 
that  of  the  limbs  in  "  claudication  intermittante." 

This  explanation  is  by  far  the  most  satisfactory  that  has 
yet  been  advanced,  and  the  cases  Huchard  instances  of  true 
angina  occurring  in  patients  suffering  from  the  rare  con- 
dition of  claudication  intermittante  are  of  great  interest. 
Whether  actual  spasm  of  the  coronary  arteries  occurs  must 
be  problematical,  and,  indeed,  from  the  thickened,  rigid 
condition  of  their  walls  in  many  cases,  it  would  scarcely 


ANGINA   PECTORIS.  37 1 

seem,  to  be  possible.  But  the  suggestion  that  the  relatively- 
deficient  blood  supply  to  the  heart  muscle  through  the 
diseased  coronary  vessels  induces  a  condition  akin  to  cramp 
of  the  heart  when  it  is  called  upon  to  do  extra  work  will 
explain  the  occurrence  of  angina  in  all  the  diverse  patho- 
logical conditions  of  the  heart  with  which  it  may  be 
associated. 

We  must,  it  seems  to  me,  assume  that  it  is  one  of  the 
arrangements  by  which  the  adjustment  of  internal  reactions 
to  external  conditions  is  secured.  The  existence  of  the 
patient  is  threatened  at  the  moment  of  the  attack  by  arrest 
of  the  heart's  action,  and  were  it  not  for  the  warning  given 
by  the  pain,  and  the  cessation  of  exertion  thus  enforced, 
the  subject  of  this  particular  affection  of  the  heart  would 
die  suddenly  without  any  warning. 

Diagnosis. 

Angina  pectoris  may  be  closely  simulated  by  paroxysms 
of  pain  which  are  not  symptomatic  of  disease  of  the  heart 
of  any  kind,  and  are  not  attended  with  danger,  and,  as  we 
usually  have  to  depend  on  the  account  given  by  the 
patient,  it  is  often  a  matter  of  great  difficulty  to  distinguish 
between  true  angina  and  merely  anginoid  attacks.  The 
difficulty  will  sometimes  be  aggravated  by  the  fact  that  the 
patient  has  carefully  read  up  the  symptoms. 

The  age  of  the  subject  may  be  of  assistance  in  deter- 
mining the  question.  Angina  is  very  rare  before  the  age 
of  forty-five,  except  in  the  case  of  aortic  valvular  disease  or 
aneurysm  or  aortitis. 

Sex,  again,  may  often  enable  us  to  exclude  angina 
without  hesitation.  It  is  extremely  rare  in  women  at  any- 
period  of  life  in  the  absence  of  the  conditions  just  enume- 
rated, whereas  so-called  angina  is  a  favourite  complaint  of 
neurotic  ladies  at  all  ages  above  thirty.     What  is  described 


372  HEART  DISEASE. 

as  "  spasms  "  by  tea-drinking  female  out-patients  becomes 
angina  among  the  educated  and  neurotic. 

The  appearance  of  the  patient  as  ascertained  from  friends 
who  have  witnessed  attacks  may  be  valuable  evidence.  It 
does  not  necessarily  follow  that  if  he  turns  pale  and  has  a 
look  of  alarm  and  suffering  the  paroxysms  are  those  of  true 
angina ;  but  if  his  colour  and  expression  show  no  change 
it  will  be  evidence  to  the  contrary. 

The  circumstances  under  which  the  early  attacks  come 
on  are  very  significant.  With  rare  exceptions  the  pain  of 
angina  is  first  experienced  during  exertion,  and  when  it 
gradually  increases  in  intensity  with  each  successive  attack 
and  is  provoked  more  and  more  readily,  there  can  be  little 
doubt  as  to  its  nature.  If,  on  the  other  hand,  the  first 
paroxysms  set  in  during  repose,  and  particularly  at  a  given 
interval  after  food,  or  at  a  particular  hour  of  the  night,  the 
inference  is  equally  strong  that  they  are  pseudo-anginal  in 
character  and  of  gastric  origin.  Unless  the  history,  onset, 
and  nature  of  the  paroxysms  are  quite  characteristic,  and 
confirmatory  physical  signs  are  present,  we  should  only 
make  a  definite  diagnosis  of  angina  when  all  possible 
explanation  of  the  pain  can  be  excluded. 

If  we  leave  out  of  the  consideration  neurotic  and 
hysterical  attacks,  which  are  usually  easily  recognizable, 
the  cause  of  the  spurious  angina  is  nearly  always  some 
functional  derangement  of  the  stomach,  and  evidences  of 
disturbance  of  the  digestion,  such  as  occasional  attacks  of 
vomiting,  habitual  flatulency  with  eructation,  will  often  aid 
in  establishing  the  distinctive  diagnosis.  In  many  cases 
dilatation  of  the  stomach  may  be  demonstrable  by  percus- 
sion and  succussion. 

A  common  combination  is  dilatation  or  distension  of  the 
stomach  and  high  arterial  tension.  Together  they  give  the 
nearest  imitation  of  true  angina,  and  if  the  heart  be  at  all 
weak  a  fatal  result  is  by  no  means   impossible   in  elderly 


ANGINA   PECTORIS.  373 

subjects.  Such  a  result  may  be  invited  if  the  functional 
derangement  of  the  stomach  and  liver  are  ignored,  and 
digitalis  or  other  cardiac  tonic  is  given  or  the  Schott  treat- 
ment adopted,  or  if  the  paroxysms  are  simply  treated  by 
nitrite  of  amyl  or  nitro-glycerine. 

The  following  case  may  be  given  to  illustrate  these  attacks  of 
so-called  "Pseudo-angina."  A  medical  man,  aged  52,  consulted  me 
for  sudden  and  agonizing  attacks  of  pain  in  the  prsecordial  area. 
They  were  so  severe  that  he  had  to  sit  down  and  lean  forward,  and 
was  incapable  of  movement  or  speech  while  they  lasted.  He  himself 
attributed  them  to  angina  pectoris,  but  found  that  trinitrin  or  nitrite 
of  amyl  gave  no  relief.  He  was  a  gouty  subject,  and  had  had  several 
attacks  of  acute  articular  gout,  and  some  of  his  medical  friends  attri- 
buted the  anginoid  pain  to  gout.  I  found,  on  examination,  that  the 
vessels  were  in  good  condition,  the  arterial  tension  was  not  high, 
there  was  no  valvular  disease  of  the  heart,  which  was  normal  in  size  ; 
and  that  the  heart  sounds  were  good.  On  examining  the  abdomen,  I 
found  that  there  was  enormous  dilatation  of  the  stomach,  and,  on 
questioning  him,  ascertained  that  he  was  a  heavy  feeder,  and  was  in 
the  habit  of  eating  large  quantities  of  meat  and  drinking  effervescing 
water  with  whisky  at  lunch  and  dinner.  I  also  ascertained  that  the 
attacks  of  pain  did  not  come  on  after  exertion  or  exposure  to  cold,  but 
usually  after  a  full  meal.  Taking  all  these  matters  into  consideration, 
I  came  to  the  conclusion  that  the  attacks  were  not  those  of  true 
angina  pectoris.  I  enjoined  moderation  in  diet,  the  giving  up  of 
effervescing  water,  and  limitation  in  the  amount  of  fluids  taken,  and 
prescribed  a  mercurial  purge  once  a  week.  The  attacks  soon  ceased, 
and  have  never  recurred,  and  though  he  has  since  had  several  bouts 
of  acute  gout,  he  is  now  in  good  health,  and  it  is  ten  years  since  the 
attacks  of  precordial  pain  for  which  he  consulted  me. 


Prognosis. 

The  prognosis  of  angina  is  beset  with  uncertainty.  We 
can  never  tell  when  the  next  attack  will  come  on,  or 
whether  it  may  not  be  the  last.  We  are  not,  however, 
altogether  without  guidance,  the  elements  of  which  will  be 
an  estimate  of  the  relative  predominance  of  the  two  chief 
factors  in  the  production  of  the  attack — whether  inherent 
weakness  of  the  heart  wall  on  the  one  hand,  or,  on  the  other. 


374  HEART  DISEASE. 

obstruction  in  the  circulation  or  other  cause  of  embarrass- 
ment of  the  heart's  action. 

V/hile  the  attacks  only  come  on  when  provoked  by- 
considerable  exertion  or  excitement,  or  by  flatulent  in- 
digestion (not,  of  course,  taking  the  patient's  word  for  the 
last-named  cause),  the  hope  may  be  entertained  that  by 
care  in  avoiding  all  known  occasions  they  may  be  post- 
poned indefinitely.  If,  further,  there  is  habitual  high 
tension  in  the  pulse,  as  in  "angina  vasomotoria,"  this  is 
at  the  same  time  evidence  of  obstruction  in  the  arterioles 
and  capillaries  which  may  be  capable  of  mitigation  by 
treatment,  and  of  some  degree  of  vigour  in  the  heart,  which 
will  usually  be  hypertrophied.  So  also  will  be  accentuation 
of  the  aortic  second  sound,  and  still  more  any  recognizable 
impulse  or  apex  beat. 

The  patient,  of  course,  must  not  take  exercise  imme- 
diately after  food,  must  never  hurry  or  walk  against  a 
wind,  and  even  on  level  ground  must  adapt  his  pace  to  his 
condition,  and  if  compelled  to  go  uphill  must  do  so  very 
gently  and  circumspectly. 

Angina,  again,  in  connection  with  aortic  valvular  dis- 
ease, may  run  a  very  protracted  course.  It  is  when  the 
pulse  is  soft  and  the  heart  is  normal  in  dimensions,  with 
imperceptible  impulse  and  weak  sounds,  as  in  fatty  degene- 
ration— when,  in  fact,  the  results  of  careful  examination  are 
negative — that  the  greatest  uncertainty  and  danger  exist. 
The  occurrence  of  unprovoked  attacks  and  of  nocturnal 
angina  will  emphasize  this  conclusion. 

Treatment. 

The  primary  significance  of  angina  pectoris  is,  as  has 
been  said,  that  the  heart  is  unequal  to  the  task  of  pro- 
pelling the  blood.  The  heart  is  itself  always  in  fault,  but 
undue  resistance  in  the  vessels  may  play  an  important  part 


ANGINA  PECTORIS.  375 

in  the  production  of  the  pain.  The  first  consideration' 
therefore,  when  the  treatment  of  angina  is  undertaken,  will 
be  whether  there  is  arterio-capillary  obstruction  which  can 
be  removed.  The  pulse  will  be  examined  carefully  and 
repeatedly  at  different  periods  of  the  day,  before  and  after 
food,  before  and  after  the  night's  rest,  before  and  after  such 
exercise  as  the  patient  can  take  with  impunity.  If  at  any 
time  the  artery  is  distinctly  full  between  the  beats,  virtual 
tension  exists,  i.e.  there  would  be  tension  were  there  adequate 
vis  a  tcrgo,  and  it  may  be  concluded  that  obstruction  is 
present  in  the  arterioles  and  capillaries  which  probably 
contributes  to  the  embarrassment  of  the  enfeebled  heart, 
the  removal  of  which  may  afford  relief.  Not  uncommonly 
there  will  be  found  a  well-marked  senile  pulse,  with  the 
arteries  large,  tortuous,  and  thickened,  full  between  the 
beats,  but  compressible,  the  pulse  wave  being  sudden  and 
unsustained.  Here  the  loss  of  elasticity  and  expansibility 
of  the  entire  arterial  tree  will  be  a  cause  of  difficulty  to 
the  heart.  The  aortic  trunk  and  its  main  branches  being 
atheromatous  and  refusino-  to  dilate  Avhen  the  blood  is 
propelled  into  them,  the  systole  encounters  the  peripheral 
resistance  at  once  just  as  if  the  vessels  were  a  system  of 
rigid,  inelastic  tubes.  Nothing  can  be  done  to  remedy  /the 
degeneration  of  the  arteries,  but  it  may  be  possible  to  lessen 
the  resistance  in  the  capillary  net-work  which  has  been  a 
chief  factor  in  the  production  of  the  atheromatous  state, 
and  which  is  now  adding  cardiac  overstrain  and  angina 
to  previous  ill-effects. 

In  some  cases  of  angina  the  pulse  has  all  the  characters 
of  high  tension  without  advanced  disease  of  the  vessels. 
This  will  usually  be  in  gouty  subjects,  and  we  have  angina 
which  may  justly  be  called  "  gouty." 

Whenever  high  arterial  tension  can  be  distinctly  recog- 
nized in  angina  pectoris,  there  is  an  opening  for  treatment 
which  may  be  palliative  to  a  very  important  extent,  and 


376  HEART  DISEASE. 

sometimes  curative.  The  treatment  will  be  such  as  has 
already  been  described  in  discussing  high  arterial  tension. 
Colchicum  may  be  given  with  the  mercurial  aperient  in 
gouty  angina,  and  also  a  mixture  containing  iodide  and 
bicarbonate  or  citrate  of  potash,  with  gentian  or  some 
other  vegetable  bitter  tonic,  twice  or  three  times  a  day. 
The  iodide  when  well  borne  is  often  of  remarkable  service. 
In  such  cases  the  treatment  may  be  pursued  with  con- 
fidence and  with  a  certain  degree  of  vigour.  The  diet 
must  be  strictly  regulated,  and  the  nearer  it  can  be  brought 
to  a  milk  and  farinaceous  diet  without  incurring  distension 
of  the  stomach  and  flatulent  dyspepsia  the  better.  Heavy 
meals  must,  of  course,  be  avoided.  Elimination  may  be 
furthered  by  a  tumbler  of  Vichy  or  Evian  water,  or  plain 
soft  water  night  and  morning. 

When  there  is  no  conspicuous  tension  in  the  arteries, 
and  their  walls  are  in  a  state  of  degeneration,  and  when 
with  this  the  walls  of  the  heart  are  weak  and  probably 
fatty,  while  the  same  end  is  held  in  view  and  similar  means 
are  put  in  operation,  great  caution  and  watchfulness  must 
be  exercised.  The  bowels  must  be  made  to  act  daily,  but 
mercurial  aperients  must  be  sparingly  employed,  an  aloetic 
pill  or  liquorice  powder,  or  some  preparation  of  cascara, 
being  given,  if  necessary,  in  the  intervals. 

When  angina  complicates  disease  of  the  aortic  valves, 
it  is  difficult  to  say  whether  arterio-capillary  resistance  con- 
tributes in  any  way  to  its  production,  but  if  the  pulse  is 
good  it  will  be  well  to  give  mild  mercurial  aperients  and 
iodides  on  the  assumption  that  such  may  be  the  case,  though 
caution  must  be  observed  in  their  administration. 

If  the  pulse  in  the  intervals  between  the  attacks  of 
anginoid  pain  is  small,  short,  easily  compressible  and 
destitute  of  tension,  no  good  result  is  to  be  expected  from 
eliminant  treatment,  and  even  small  doses  of  mercury  may 
depress  the  patient. 


ANGINA   PECTORIS.  377 

Prominence  has  been  given  to  removal  of  arterio-oapil- 
lary  resistance  by  eliminant  treatment,  because  when  called 
for,  it  may  yield  more  permanent  relief  than  any  other 
line  of  treatment ;  but  arsenic  and  phosphorus  may  render 
very  important  service,  and  except  in  cases  of  markedly 
high  arterial  tension  one  or  other  of  these  should  be 
given  concurrently  with  eliminants.  A  particularly  useful 
combination  is  arsenic  with  iodide  of  potassium  and  nux 
vomica.  Phosphorus  seems  to  have  a  specially  fa\rourable 
effect  in  angina  associated  with  aortic  regurgitation.  Bella- 
donna or  cannabis  indica  may  be  useful  adjuvants  in  some 
cases ;  quinine  and  nux  vomica  also  are  often  of  service. 
Nitro-glycerine  or  the  heavier  nitrites  may  also  be  required 
habitually,  though  it  is  best  when  possible  to  reserve  their 
use  for  the  anginoid  attacks  themselves.  In  the  case  of  a 
medical  friend  the  erythrol  tetranitrate  appeared  to  be  of 
great  service,  enabling  him  to  avert  a  fatal  attack  for 
many  years. 

Treatment  op  the  Attacks. 

There  remains  to  be  considered  the  treatment  of  the 
attacks  themselves.  Formerly  brandy,  various  combinations 
of  ether,  nitrous  ether,  ammonia,  lavender,  and  camphor, 
were  the  chief  drugs  resorted  to.  Inhalation  of  amyl 
nitrite  and  the  administration  of  nitro-glycerine  or  of 
sodium  nitrite  or  erythrol  tetranitrate  have  now  almost 
entirely  superseded  these  remedies. 

Whatever  the  remedy,  the  patient  should  always  carry 
it  about  with  him,  and  have  recourse  to  it  as  soon  as  the 
pain  really  sets  in.  The  amyl  nitrite  is  supplied  in  the 
convenient  form  of  glass  capsules  containing  five  mins., 
enclosed  in  a  silk  bag,  so  that  one  of  these  can  be  broken 
in  a  handkerchief  and  the  vapour  inhaled.  Some  prefer 
to    carry  a  small  bottle  of  amyl  nitrite  about,  to  which 


37§  HEART  DISEASE. 

they  can  have  recourse  when  the  attack  threatens.  Nitro- 
glycerine, however,  taken  by  the  mouth,  appears  to  be 
more  generally  useful,  since,  though  the  effect  is  scarcely  as 
rapid  as  that  of  inhaled  amyl  nitrite,  it  lasts  much  longer. 
Erythrol  tetranitrate  is  even  more  satisfactory,  as  its  effects 
are  more  prolonged  than  those  of  trinitrin.  Tabloids  of 
nitro-glycerine  containing  one  min.  of  a  one  per  cent, 
solution  can  be  carried  about,  and  one  or  two  can  be 
swallowed  when  necessary  with  very  little  loss  of  time. 

In  most  cases  nitro-glycerine  has  a  better  effect  than 
amyl  nitrite,  though  in  rare  instances  nitro-glycerine  ap- 
pears to  have  no  influence  on  the  spasm  to  which  nitrite 
of  amyl  at  once  gives  relief.  In  two  cases  of  the  kind 
that  I  have  seen,  it  has  seemed  to  me  extremely  probable 
that  the  anginoid  paroxysm  had  its  origin  in  the  right 
ventricle. 

Occasionally  when  the  nitrites  fail  we  have  to  fall  back 
on  the  old-fashioned  remedies,  especially  when  the  heart 
failure  is  pronounced  and  the  pulse  tension  is  extremely 
low.  Here  it  may  do  more  good  to  help  the  heart  by 
stimulants  than  to  relieve  it  of  work.  While  the  paroxysms 
of  angina  are  for  the  most  part  brief,  the  agony  being  such 
that  it  seems  as  if  another  moment  must  prove  fatal,  there 
are  at  times  attacks  of  a  protracted  character.  When  the 
pain  persists  in  spite  of  nitrites  and  stimulants,  morphine 
and  atropine  should  be  administered  hypodermically,  and 
it  is  well  to  carry  the  needle  into  the  substance  of  a  muscle 
where  the  circulation  is  more  active  than  in  the  sub- 
cutaneous cellular  tissue.  The  initial  dose  should  be  small, 
but  it  may  be  necessary  to  employ  morphine  boldly.  A 
turpentine  stupe  may  also  be  applied  over  the  region  of 
the  heart,  or  a  mustard  leaf  or  poultice. 

It  must  be  remembered  also  that  the  nitrites  give  rise  to 
great  frequency  of  the  heart  action  which  may  be  a  source 
of  distress.     We    should  consequently  employ  them  very 


ANGINA   PECTORIS.  379 

cautiously  wheu  the  augina  is  accompanied  by  a  frequent 
pulse.  The  nitrites  have  been  supposed  to  be  heart  tonics, 
but  while  their  most  prominent  action  is  relaxation  of  the 
arterio-capillary  net-work  they  also  relax  the  cardiac 
muscular  fibres. 

As  in  so  many  other  instances,  the  employment  of  nitro- 
glycerine and  the  nitrites  is  not  without  its  drawbacks. 
Patients  often  come  to  rely  on  the  immunity  from  pain 
which  the  remedies  confer  and  then  presume  upon  it. 
Liberties  are  taken  and  imprudences  are  committed,  so  that 
not  unfrequently  sudden  death  is  precipitated  which  might 
with  care  have  been  staved  off  for  years.  In  placing  the 
remedy  in  the  patient's  hands,  therefore,  emphatic  words 
of  caution  must  be  spoken  and  the  danger  must  be 
pointed  out. 

The  instructions  to  be  given  with  regard  to  exercise  are 
extremely  important.  After  a  very  severe  paroxysm,  how- 
ever provoked,  rest  in  bed  may  be  necessary  for  some  days, 
and  even  for  a  period  of  two  or  three  weeks,  if  the  attack 
has  been  prolonged.  The  heart  may  be  left  extremely  weak, 
its  action  slow  or  faltering  and  irregular,  and  the  sounds 
scarcely  audible,  and  sitting  up  or  turning  in  bed  may  be 
attended  with  giddiness  or  faintness  or  pain  in  the  region 
of  the  heart.  When  such  conditions  are  present,  time  must 
be  given  to  the  heart  to  recover  itself,  and  measures  must 
be  taken  to  relieve  flatulence  and  constipation,  which  will 
probably  be  associated  with  the  other  symptoms. 

Under  ordinary  circumstances,  however,  the  rule  usually 
applicable  in  heart  disease  holds  good  here.  Whatever 
exercise  the  patient  can  take  without  provoking  an  attack 
at  the  time,  or  prostration  afterwards,  he  will  be  the  better 
for.  While,  however,  the  exercise  should  be  as  regular 
as  possible,  in  no  case  is  it  more  necessary  to  bear 
in  mind  the  fact  that  the  capacity  for  exertion  varies  from 
day  to  day,  and  that  the  sufferer  from  angina  can  do  easily 


3§o  HEART  DISEASE. 

one  day  what  would  be  impossible  for  hirn  on  another. 
This  is  one  of  the  objections  to  the  (Ertel  methods  of 
treatment.  Some  of  the  influences  which  affect  him  we  can 
recognize,  such  as  wind,  or  severe  cold,  or  great  heat,  or 
weather  which  is  felt  by  people  in  health  to  be  oppressive, 
or  a  moisture-laden  atmosphere  ;  others  arise  out  of  internal 
conditions,  flatulence,  dyspepsia,  constipation,  functional 
derangements  of  the  liver.  The  patient's  feelings  and  in- 
clinations have  thus  to  be  taken  into  account,  but  without 
allowing  inertia  or  nervousness  to  have  undue  weight. 
There  is  great  room  here  for  judgment  and  tact  and  per- 
sonal knowledge  of  the  patient's  disposition.  Besides  the 
caution  necessary  in  cold  and  hot  weather,  the  liability  to 
anginoid  attacks  on  walking  soon  after  food  must  be  borne 
in  mind,  and  a  period  of  rest  after  meals  must  be  enjoined, 
esj^ecially  after  that  particular  meal  which  experience  in  the 
case  under  treatment  has  shown  to  be  worst  in  this  respect. 


CHAPTEE   XXVI. 

FUNCTIONAL  AFFECTIONS   (SO-CALLED)   OF 
THE  HEAET. 

PAIN  IN  PRECORDIAL  REGION— SITE  OF  PAIN — EXPLANA- 
TION OP  REFERRED  PAIN  AND  AREAS  OF  CUTANEOUS 
HYPERALGESIA  —  DISORDERS  OF  RHYTHM  OF  THE 
HEART  —  MECHANISM  BY  WHICH  THE  RHYTHM  OF 
THE  HEART  IS  REGULATED  —  INTERMITTENT  AND 
IRREGULAR  ACTION  OF  THE  HEART  —  PALPITATION  : 
TACHYCARDIA. 

The  term  "  functional  affections "  is  retained,  not  for  any 
merit  of  its  own  but  for  want  of  a  better.  Under  it  must  be 
discussed  a  variety  of  symptoms  having  the  heart  for  their 
centre,  but  which  cannot  be  assigned  to  any  structural 
change.  Taken  all  together  they  give  rise  to  much  actual 
suffering,  and  to  far  more  nervous  apprehension  and  fear 
of  death  than  definite  valvular  and  structural  disease  com- 
bined. So  much  is  this  the  case  that  when  patients  come 
complaining  of  the  heart,  we  are  almost  safe  in  concluding 
that  the  heart  is  disturbed  by  some  cause  outside  itself  and 
is  not  the  seat  of  disease. 


Cardiac  Pain. 

Pain  is  one  of  the  symptoms  which  frequently  gives  rise 
to  apprehension  of  heart  disease.  Leaving  out  of  the 
question  that  of  angina,  which  has  already  been  discussed, 


382  HEART  DISEASE. 

its  most  common  seat  is  the  region  of  the  apex,  but  it 
may  be  felt  over  any  part  of  the  cardiac  area,  the  left 
third  space  being  next  to  the  apex,  the  most  frequent  part 
in  which  pain  is  experienced.  It  is  most  commonly  of  a 
dull  aching  character,  but  may  be  sharp  and  stabbing  or 
burning,  and  nervous  women  will  exhaust  all  the  epithets 
which  can  be  applied  to  pain  in  their  description  of  their 
sufferings.  Tenderness  on  pressure  very  commonly  accom- 
panies the  pain;  it  is  superficial  and  is  equally  severe, 
whether  the  pressure  is  made  over  a  rib  or  in  an  intercostal 
space  ;  it  is  often  particularly  severe  in  the  edge  of  the 
mamma  when  this  extends  into  the  tender  area.  The 
tenderness  is  quite  extra-thoracic,  and  is  felt  when  the  heart 
is  not  even  indirectly  reached  by  the  pressure. 

Another  special  seat  of  tenderness  is  over  the  second  rib, 
about  an  inch  from  the  edge  of  the  sternum,  where  a  branch 
of  the  cervical  plexus  crosses  the  rib.  Pressure  here  not 
only  causes  pain,  but  may  give  rise  to  intolerable  cardiac- 
distress. 

Explanation  of  Referred  Pain  and  Areas  of  Hyperalgesia. — 
The  relationship  of  areas  of  cutaneous  hyperalgesia  and 
referred  pain  to  visceral  affections  has  been  ably  demon- 
strated by  Mackenzie  *  and  by  Head,t  and  will  explain 
most  of  the  above  phenomena.  Briefly,  Head's  conclusions 
are  as  follows  : — 

As  the  viscera  are  insensitive,  and  from  their  inacces- 
sibility to  touch  are  incapable  of  developing  the  sense  of 
localization,  the  maximum  pain  is  not  felt  in  the  affected 
organ.  A  painful  stimulus  to  an  internal  organ  is  con- 
ducted to  the  corresponding  segment  of  the  cord,  where  it 
comes  into  contact  with  the  sensory  nerves  from  the  area  of 
the  body  supplied  by  the  same  segment.  The  sensory  and 
localizing  power  of  the  skin  is  enormously  in  excess  of  that 

*  Med.  Chron.,  Manchester,  1892,  p.  293;  and  Lancet,  1895,  vol.  i.  p.  1G. 
f  Brain,  1893,  pp.  1  et  seq. ;  and  J894,  pp.  339  et  seq. 


CARDIAC  PAIN.  383 

of  the  viscera,  and  by  a  psychical  error  of  judgment  the 
pain  is  referred  to  the  corresponding  segmental  area  of  the 
body,  instead  of  to  the  affected  organ. 

In  neuroses  of  the  heart,  hyperesthesia,  or,  as  Head  puts 
it,  hyperalgesia,  of  the  corresponding  cutaneous  segmental 
areas  is  a  common  feature,  whereas  in  angina  pectoris  this 
is  as  nothing  compared  with  the  widespread  agonizing 
referred  pain. 

According  to  Mackenzie  and  Head,  in  most  affections 
of  the  heart  and  aorta  the  cutaneous  areas  in  which  hyper- 
algesia is  present,  and  to  which  the  pain  is  referred,  are 
those  corresponding  to  the  first,  second,  third,  and  fourth 
dorsal  segments,  which  comprise,  roughly,  all  the  front  of 
the  chest,  from  the  second  rib  to  the  level  of  the  nipple, 
the  posterior  and  lateral  surface  from  the  level  of  the  seventh 
cervical  to  the  fourth  dorsal  spine,  and  certain  areas  on  the 
inner  aspect  of  the  arms. 

In  angina  pectoris,  however,  the  distribution  of  the 
referred  pain  differs  considerably  from  that  in  other  affec- 
tions of  the  heart,  and  it  would  appear  that  the  painful 
stimulus  to  the  heart  is  so  severe  that  it  sets  up  a  wide- 
spread and  violent  commotion  in  the  cord,  so  that  pain  may 
be  referred  upwards  over  certain  cervical  areas  and  down- 
wards as  low  as  the  ninth  dorsal  segmental  area. 

Etiology. — Pain  in  the  region  of  the  heart  may  be  due  to 
conditions  of  the  heart  itself,  to  dilatation  or  overstrain, 
to  an  enfeebled  and  irritable  state  after  a  depressing- 
illness,  or  to  toxic  influences,  e.g.  tobacco,  to  direct  pressure 
upon  the  heart  by  a  dilated  stomach  or  extreme  distension 
of  the  abdomen,  to  reflex  disturbance  from  some  visceral 
derangement,  or  to  nervous  or  emotional  states. 

Taking  the  last-named  first,  it  is  exemplified  by  the 
sharp  pain  in  the  heart,  which  may  be  induced  by  a  sudden 
shock  or  fright,  or  by  powerful  emotion,  and  by  the  heart- 
ache of  profound  or  protracted  grief.    But,  without  adequate 


384  HEART  DISEASE. 

emotional  influence  nothing  is  more  common  than  cardiac 
pain  as  an  expression  of  nervous  depression. 

Eeflex  pains  are  mostly  of  dyspeptic  origin,  but  may  be 
associated  with  uterine  derangements.  The  pain  caused  by 
direct  pressure  of  the  diaphragm,  carried  upwards  by  a 
dilated  stomach  or  distension  of  the  colon  or  intestine 
generally,  is  accompanied  by  oppression  of  the  breathing, 
and  is  usually  felt  at  the  base  of  the  heart  and  is  aggravated 
on  lying  down. 

Pain  due  to  overstrain  of  the  heart  is  commonly  a  diffuse 
ache  over  the  cardiac  area,  generally  accentuated  in  the 
region  of  the  apex. 

The  treatment  of  cardiac  pain  will  in  its  details  vary 
with  the  cause.  If  due  to  toxic  influences,  these  should 
be  removed.  If  due  to  overstrain  or  dilatation,  the  treat- 
ment should  be  on  the  lines  given  on  p.  303.  But  in 
all  cases  it  is  most  important  to  be  able  to  convince  the 
patient  that  there  is  no  disease.  While  he  has  the  idea 
in  his  mind  that  he  is  suffering  from  some  serious  heart 
affection,  the  concentration  of  his  attention  on  the  heart 
will  be  sufficient  to  renew  the  pain,  and  his  apprehensions 
will  interfere  with  the  recovery  of  his  nervous  equilibrium. 

If  due  to  reflex  disturbances,  such  as  derangements 
of  the  digestive  organs,  liver  or  uterus,  these  should  be 
rectified  by  suitable  diet  and  treatment,  and,  as  a  rule, 
tonics  will  be  of  service. 

With  the  internal  and  general  remedies  the  local 
application  of  belladonna  as  a  liniment  or  plaster  will  be 
useful.  The  plaster  is  often  more  efficacious  if  it  is  applied 
so  as  to  afford  support  or  to  exercise  pressure  on  the  painful 
part,  and  it  is  well,  therefore,  to  apply  it  in  strips. 
Counter-irritation  over  the  tender  area  by  a  mustard-leaf 
or  blisters  is  often  of  great  service  in  neurotic  individuals. 


mechanism  regulating  rhythm  of  the  heart.    385 

Disorders  of  Ehythm  of  the  Heart. 

These  may  be  classified  under  the  following  heads  ; — 

1.  Interniittency  of  the  heart's  action. 

2.  Irregularity  in  the  force  and  frequency  of  the  heart 
beats. 

3.  Abnormally  rapid  action  of  the  heart,  which  may  be 
temporary  (palpitation)  or  continuous  (tachycardia). 

4.  Abnormally  slow  action  of  the  heart  (bradycardia). 
These  will  be  discussed  in  detail  under  their  respective 

headings  ;  but  it  may  be  as  well  first  to  briefly  refer  to  the 
views  held  as  to  the  mechanism  by  which  the  rhythm  of 
the  heart  is  regulated. 

Mechanism  regulating  the  Ehythm  of  the  Heart. 

Gaskell  *  describes  the  functions  of  the  muscular  fibres 
of  the  heart  as  rhythmicity,  excitability,  contractility,  con- 
ductivity, and  tonicity,  by  virtue  of  which  the  heart  is  able 
to  beat  and  keep  up  the  circulation  independently  of  nerve 
control,  the  vagus  and  sympathetic  having  only  a  moderating 
influence  upon  these  varied  functions. 

The  muscle  fibres  at  the  mouth  of  the  great  veins  and 
adjoining  portion  of  the  right  auricle,  and  the  muscular 
tissue  joining  the  auricles  and  ventricles,  according  to 
Gaskell,  possess  the  greatest  power  of  automatically  creating 
a  stimulus  for  contraction. 

The  fibres  joining  the  auricle  and  ventricle  play  an 
important  part  in  the  conduction  of  the  stimulus  for  con- 
traction from  auricle  to  ventricle.  On  applying  a  clamp  to 
the  auriculo- ventricular  groove  in  a  frog's  heart,  Gaskell 
states  that,  according  to  the  tightness  of  the  clamp,  the 
ventricle  may  be  made  to  respond  to  every  second,  third,  or 
fourth  contraction  of  the  auricle. 

*  "  Text-book  of  Physiology,"  edited  by  Scbafer,  vol.  ii. 

2c 


386  HEART  DISEASE. 

Mackenzie,*  in  a  valuable  paper,  calls  attention  to  these 
facts,  and  to  the  work  of  Englemann  and  Wenckebach  on 
disordered  rhythm  of  the  heart,  and  contributes  a  series  of 
interesting  observations  on  the  nature  of  the  conducting 
power  whereby  the  stimulus  is  conveyed  from  auricle  to 
ventricle.  His  method  of  investigation  is  to  take  simul- 
taneous tracings  of  the  jugular  and  carotid  or  radial  pulses, 
and  thus  time  the  period  which  elapses  between  the  auri- 
cular and  ventricular  systole. 

He  attaches  great  importance  to  the  function  of  the 
muscle  fibres  connecting  the  auricle  with  the  ventricle,  and 
shows  that  certain  forms  of  arrhythmia,  more  especially 
intermittent  action  of  the  heart  and  bradycardia,  are  pro- 
bably due  to  depression  of  or  a  block  in  the  conductivity  of 
these  fibres. 

Nervous  Influences. — Though  the  rhythmic  action  of  the 
heart  is  automatic  and  dependent  on  the  inherent  properties 
of  its  muscular  fibres,  the  central  nervous  system  exercises 
an  important  controlling  influence  on  the  varied  functions 
of  the  cardiac  muscle  through  the  pneumogastric  and  sym- 
pathetic nerves.  Messages  must  constantly  be  passing  to 
and  fro  along  these  nerves  between  the  heart  and  centres 
in  the  medulla,  by  means  of  which  the  heart  is  kept  in- 
formed of  the  condition  and  requirements  of  the  body  in 
general,  and  the  vascular  system  in  particular,  so  that  the 
force  and  frequency  of  its  beat,  and  the  degree  of  tonicity 
of  its  muscle  fibres,  are  regulated  accordingly. 

All  are  familiar  with  the  extreme  and  distressing  varia- 
tions in  the  frequency  of  the  heart  beat  which  may  be 
induced  by  sudden  and  violent  emotions  of  fear  or  anger, 
or  by  intense  excitement,  which  in  certain  diseased  con- 
ditions may  give  rise  to  a  fatal  syncopal  attack  by  arrest 
of  the  heart's  action.  Disturbances  of  rhythm  may  be 
occasioned  by  reflex  impulses  transmitted  from  the  stomach 
*  "  New  Methods  of  Studying  Affections  of  the  Heart,"  B.M.J.,  March,  1D05. 


INTERMITTENCY  OF  THE   PULSE.  387 

or   other   viscera    in   consequence   of   functional   derange- 
ments. 

G-ibson,*  in  his  excellent  account  of  "  Nervous  Affec- 
tions of  the  Heart,"  gives  some  interesting  tracings  from 
the  experimental  work  of  Wenckebach  and  Cushny,  which 
show  the  different  effects  of  electrical  stimuli  on  the  rhythm 
of  the  heart,  according  to  the  region  stimulated,  and  the 
time  in  the  cardiac  cycle  at  which  they  are  applied. 

As  one  of  the  results  of  these  experiments,  it  is  demon- 
strated that  if  a  stimulus  is  applied  to  the  heart  just  before 
the  normal  of  contraction  is  due,  a  premature  imperfect 
systole  takes  place,  which  is  insufficient  to  transmit  a 
pulse  wave  to  the  wrist,  so  that  a  beat  is  dropped  in  the 
radial  pulse.  This  will  explain  certain  forms  of  inter- 
mittent pulse  and  irregular  action  of  the  heart.  The 
nature  of  the  stimulus  which  interferes  with  the  normal 
automatic  contraction  of  the  heart  is  not  always  easy  to 
determine.  Probably,  when  the  intermittency  is  a  tem- 
porary phenomenon,  it  is  the  result  of  a  reflex  from  some 
gastric  or  other  visceral  disturbance.  When  persistent, 
it  may  perhaps  be  due,  not  to  reflex  nervous  influences, 
but  to  a  block  in  the  conductivity  of  certain  of  the  cardiac 
muscle  fibres  referred  to  above. 

Intebmittency  of  the  Pulse. 

By  an  intermittent  pulse  is  meant  a  pulse  in  which  a 
beat  is  missing  from  time  to  time,  while  in  the  intervals  it 
is  perfectly  regular.  The  intermission  may  occur  at  regular 
and  definite  periods  every  four,  six,  or  more  beats  up  to 
twenty,  or  the  number  of  intervening  pulsations  may  vary. 

It  is  not  characteristic  of  any  form  of  heart  affection  and 
is  rarely  indicative  of  organic  disease.  An  intermittent 
pulse  may  be  constant  and  habitual,  and  the  intermission 

*  "  Nervous  Affections  of  the  Hearf,"  Young  Pentlaud,  1904. 


388  HEART  DISEASE. 

is  then  more  likely  to  occur  at  definite  intervals ;  it  may- 
be occasional  only,  and  may  be  attributable  to  some  dis- 
turbing reflex  cause,  of  which  flatulent  dyspepsia  is  the 
most  common.  In  some  cases  the  pulse  is  intermittent 
after  each  meal ;  or  in  others  tea,  coffee,  or  tobacco  may  be 
the  special  cause  of  the  intermission.  It  is  common  also 
in  chronic  gout,  and  may  be  among  the  signs  of  fatty 
degeneration  of  the  heart.  In  case  of  doubt  the  patient 
should  be  made  to  walk  briskly  for  a  minute  or  two,  when, 
if  the  heart  is  really  weak  and  degenerated,  the  pulse  will 
falter,  whereas,  if  the  heart  is  healthy,  the  intermission  will 
usually  disappear.  Intermittency  of  pulse  may  also  be 
associated  with  nervous  debility  and  hypochondriasis,  the 
pulse  becoming  normal  again  when  the  patient  regains 
good  health.  On  examining  the  heart  it  is  usually  found 
that  the  cause  of  the  intermission  is  not  the  actual  omission 
of  a  heart  beat,  but  the  occurrence  of  a  hurried  and  im- 
perfect contraction  which  rapidly  follows  the  last  of  the 
series  of  normal  beats,  and  does  not  transmit  a  pulse  wave 
to  the  wrist.  The  imperfect  beat  may  sometimes  be  felt  on 
palpation ;  usually  only  the  first  sound  is  heard  on  aus- 
cultation at  the  apex  unaccompanied  by  a  second  sound. 
The  heart  beat  which  follows  the  intermission  is  usually 
more  powerful  than  normal.  While  it  is  the  rule  that 
there  is  this  feeble  interposed  heart  beat,  instances  occur 
where  it  cannot  be  heard  or  felt,  and  in  which  the  heart 
appears  to  remain  quite  passive.  This  condition  will  be 
discussed  further  in  the  chapter  on  bradycardia. 

The  patient  may  or  may  not  be  conscious  of  the  inter- 
mittent action  of  the  heart.  He  is  more  likely  to  be  aware 
of  it  when  it  is  symptomatic  of  some  functional  derange- 
ment than  when  it  is  habitual;  he  may  be  conscious  of  a 
vague  sense  of  discomfort  or  of  an  unpleasant  sinking 
sensation  in  the  cardiac  region  during  the  intermission,  or 
he  may  feel  the  bump  of  the  stronger  beat  which  usually 


IRREGULARITY  OF  HEART'S  ACTION.  389 

follows  the  feeble  and  imperfect  or  dropped  beat.  In  view 
of  G-askell's,  Wenckebach's,  and  Mackenzie's  work,  referred 
to  above,  the  explanation  of  intermittent  action  of  the  heart 
when  persistent  would  seem  to  be  that  it  arises  from  a 
lowering  of  conductivity  in  the  muscle  fibres  joining  the 
auricle  and  ventricle,  so  that  the  stimulus  for  contraction 
is  not  regularly  transmitted  from  auricle  to  ventricle.  Some- 
times this  may  be  attributed  to  cardiac  sclerosis,  sometimes 
there  is  no  apparent  cause.  It  may  be  met  with  in  men  who 
enjoy  vigorous  health  and  live  to  a  good  old  age.  When 
the  intermittent  action  of  the  heart  is  only  occasional,  it  is 
usually  traceable  to  some  toxic  cause,  such  as  tea,  coffee, 
or  tobacco,  or  to  reflex  gastric  or  other  visceral  disturbances, 
and  suitable  treatment  for  removal  of  the  cause  should  then 
be  adopted. 

Irregularity  of  the  Heart's  Action. 

Irregularity  of  the  heart's  action,  like  intermittency, 
may  be  habitual  or  occasional.  Habitual  irregularity  is 
commonly  present  in  mitral  incompetence  and  in  cases  of 
cardiac  dilatation  of  any  severity,  when  it  is  probably  due 
to  the  variable  supply  of  blood  to  the  left  ventricle,  as 
explained  in  Chapter  XI.  It  is  occasionally  met  with  in 
individuals  in  whom  there  is  no  evidence  of  any  heart 
disease,  and  who  enjoy  good  health  and  live  to  old  age. 
In  one  instance  I  have  known  the  heart's  action,  without 
any  apparent  cause,  to  be  markedly  irregular  during  a 
period  of  at  least  twenty  years  to  my  knowledge  in  a 
gentleman  who  lived  to  the  age  of  seventy  and  enjoyed 
vigorous  health. 

Irregularity  associated  with  excessive  frequency  of  pulse 
is  usually  of  serious  prognostic  significance,  and  may  be  an 
incident  in  the  final  stages  of  paroxysmal  tachycardia. 

Irregular  action  of  the  heart  setting  in  after  middle  life 


39°  HEART  DISEASE. 

with  evidence  of  degenerative  change  in  the  vessels  is  also 
serious,  as  it  may  be  due  to  fibroid  change  in  the  heart 
associated  with  sclerosis  of  the  coronary  vessels. 

Temporary  irregularity  of  the  cardiac  action  is  much 
more  common,  and  may  be  occasioned  by  tobacco  or  strong 
tea,  by  mechanical  embarrassment  of  the  heart  by  a  dis- 
tended stomach  or  colon,  or  by  various  reflex  causes,  such 
as  gastric  and  liver  derangements,  or  emotional  disturbances 
of  various  kinds. 

Irregularity  of  the  cardiac  action  is  more  serious  than 
intermission,  and  steps  should  at  once  be  taken  to  remove, 
if  possible,  the  exciting  cause.  When  there  is  mechanical 
embarrassment  of  the  heart  by  a  distended  and  dilated 
stomach  the  distress  at  times  may  be  severe,  and  there  is 
danger  of  a  sudden  syncopal  attack  in  elderly  people  in 
whom  the  heart  has  undergone  degenerative  changes. 

Palpitation. 

By  palpitation  is  meant  frequent  and  violent  action  of 
the  heart,  of  which  the  subject  is  conscious ;  but  patients 
will  sometimes  say  they  are  suffering  from  palpitation  when 
there  is  neither  frequency  nor  violence  recognizable  in  the 
beat  of  the  heart  or  pulse  by  the  observer,  and,  on  the 
other  hand,  may  be  unconscious  of  extremely  rapid  action 
of  the  heart  found  on  examination. 

With  palpitation  there  is  usually  uneasiness,  sometimes 
pain,  in  the  region  of  the  heart,  oppression  of  the  respiration 
with  frequent  deep  sighs  and  a  sense  of  inability  to  fill  the 
chest  sufficiently.  Often  there  is  excitement  and  alarm 
and  the  patient  feels  giddy  or  faint ;  the  face  may  be 
flushed  or  very  pale. 

When  the  heart  is  acting  very  rapidly,  many  of  the  beats 
may  fail  to  reach  the  radial  artery,  so  that  the  pulse  be- 
comes irregular.     The  reason  probably  is  that  the  ventricle 


PA  LPITA  TIOX.  39 1 

has  not  time  to  fill,  and  that  consequently  there  is  not 
sufficient  blood  propelled  into  the  aorta  to  communicate  a 
wave  to  the  peripheral  vessels.  Very  often  the  artery  is 
small  and  full  between  the  beats,  there  being  a  general 
excitement  of  the  vascular  system  with  spasm  of  the 
arterial  walls.  This  is  particularly  the  case  in  hysterical 
palpitation,  when  there  will  frequently  also  be  a  copious 
secretion  of  pale  dilute  urine. 

On   examination,  during   an   access  of  palpitation,  the 
heart  may  be  felt  to  be  beating  violently,  but    when   the 
rapidity  of  its  action  is  extreme  a  faint  vibration  only  may 
be  communicated  to  the  hand.     On  auscultation,  the  first 
sound  may  be  loud  and  short,  followed  immediately  by  a 
weak  second  sound,  or,  in  the  case  of  extreme  frequency,  the 
first  and  second  sounds  may  be  almost  identical  in  character 
and  equidistant,  resembling  very  closely  those  of  the  foetal 
heart,  and  comparable  to  the  puffing  of  a  distant  locomotive. 
Etiology. — Among  the  causes   of  what  may   be  called 
ordinary  palpitation  as  distinguished  from  tachycardia,  the 
most  important  is  a  predisposition  thereto  on  the  part  of  the 
nerve  centres  governing  the  heart,  which  may  be  inborn 
or  induced  by  modes  of  life  or  by  the  various  circumstances 
which  tend  to  lower  the  nervous  tone  or  to  promote  nervous 
excitability.     Palpitation  is  much  more  common  in  women 
than  men,  partly  in  virtue  of  the  greater  inherent  suscepti- 
bility of  the  female  nervous  system,  partly  from  the  more 
emotional  life  of  women,  their  greater  confinement  to  the 
house,  and  their  less  vigorous  exercise ;  but  child-bearing 
and   over-lactation  are  also   in   themselves  serious  predis- 
posing causes.     In  men  a  sedentary  mode  of  life,  exciting- 
occupations,   dissipatiou,   and    excesses  of  all  kinds,  over- 
indulgence in  tobacco,  bring  about  a  liability  to  palpitation. 
Mitral  stenosis  is  a  form  of  valvular  disease  in  which  attacks 
of  palpitation  are  very  liable  to  occur,  the  exciting  cause 
usually  being  gastric  disturbances. 


392  HEART  DISEASE. 

Among  the  exciting  causes  are  sudden  violent  impres- 
sions on  the  nervous  system  of  any  kind — fright,  an  un- 
expected noise,  a  startling  incident  taking  place  before  the 
eyes,  a  powerful  emotion ;  these  will  set  any  one's  heart 
beating,  but  in  a  strong  and  healthy  person  the  effect  is  of 
very  brief  duration ;  where  the  predisposition  to  palpitation 
exists  they  may  initiate  an  uncontrollable  attack.  A  similar 
statement  applies  to  exertion — a  brisk  walk  uphill  causes 
the  heart  to  act  rapidly  and  powerfully  under  normal  circum- 
stances ;  in  a  predisposed  individual  the  action  may  be 
exaggerated  and  protracted,  so  as  to  constitute  an  attack  of 
palpitation. 

But  the  characteristic  palpitation  of  the  heart  starts 
suddenly  without  obvious  exciting  cause,  while  the  patient 
is  sitting  quietly  at  work  or  reading,  or  during  sleep,  when 
he  or  she  may  wake  up  from  a  frightful  dream  which 
appears  to  have  brought  on  the  attack. 

There  is,  however,  as  a  rule,  some  internal  exciting 
cause,  which  is  most  commonly  gastric  derangement 
attended  or  not  with  flatulent  distension  of  the  stomach  or 
bowels.  Other  forms  of  peripheral  irritation  may  act  as 
exciting  causes,  such  as  uterine  affections. 

Treatment. — To  arrest  an  attack  of  palpitation  it  is 
sometimes  only  necessary  to  take  a  dozen  deliberate  deep 
breaths,  and  it  is  always  well  to  tryt  this  expedient  before 
resorting  to  drugs.  The  remedies  of  most  general  service 
are  combination  of  alkaline  and  carminative  stimulants  ; 
bicarbonate  of  soda  with  ammonia  and  camphor  or  pepper- 
mint water  is  often  sufficient,  but  compound  tincture  of 
chloroform,  ether,  valerian,  lavender,  ginger  may  be  added 
or  substituted;  in  some  cases  bromides  are  required. 
Undue  acidity  of  the  gastric  contents  is  corrected,  flatu- 
lence is  expelled,  and  possibly  the  stimulation  of  the 
pneumogastric  fibres  of  the  mucous  membrane  of  the 
stomach  may  have  some  inhibiting  influence  on  the  heart. 


TA  CHYCARDIA .  393 

Digitalis  appears  to  have  little  or  no  effect,  but  belladonna 
may  be  useful,  especially  in  combination  with  bromide  of 
ammonium  or  sodium. 

For  the  prevention  of  palpitation  the  tone  of  the  nervous 
system  must  be  raised  by  the  usual  hygienic  and  medicinal 
means,  namely,  change  to  the  seaside,  or,  better,  to  moun- 
tain health  resorts,  exercise,  fresh  air,  early  hours,  simple 
wholesome  food,  avoidance  of  undue  excitement  of  all  kinds. 
The  emplast.  belladonnas  over  the  region  of  the  heart 
appears  to  have  some  influence  in  preventing  or  moderating 
the  attack,  probably  mainly  due  to  the  mechanical  support. 

Careful  inquiry  should  be  made  as  to  any  relation 
between  the  taking  of  food  and  the  occurrence  of  an  attack 
and  as  to  the  existence  of  functional  derangements  of  the 
stomach,  liver,  or  other  organs.  The  abdomen  should  be 
examined  to  see  if  there  is  flatulent  distention  of  the 
stomach,  colon,  or  small  intestine,  and  suitable  remedies 
should  be  given  for  this,  together  with  such  tonics  as  are 
indicated  by  the  general  condition  of  the  patient. 


TACHYCARDIA. 

Attacks  of  palpitation,  or  rapid  action  of  the  heart,  may 
last  a  few  minutes  or  a  few  hours,  and  are  usually  traceable 
to  emotional  or  reflex  gastric  disturbances,  and  are  not  of 
great  severity. 

There  are,  however,  cases  in  which  rapid  action  of  the 
heart,  with  a  pulse  of  100  to  120,  is  a  more  or  less  perma- 
nent condition,  and  others  in  which  attacks  of  extremely 
rapid  action  of  the  heart,  with  from  200  to  300  beats  per 
minute,  set  in  from  time  to  time,  lasting,  perhaps,  for  several 
days,  and  eventually  proving  fatal.  To  this  latter  affection 
the  term  "  paroxysmal  tachycardia  "  lias  been  applied. 


394  heart  disease. 

Etiology. 

Occasionally  one  meets  with  individuals  in  good  health 
who  have  normally  a  pnlse  of  from  90  to  100. 

Alcoholism  in  neurotic  subjects  may  give  rise  to  a 
permanently  rapid  pulse,  and  I  have  seen  two  instances 
in  neurotic  ladies  addicted  to  alcohol  in  which  a  pulse  of 
100  to  120  was  present  for  a  considerable  number  of  years. 
A  retired  naval  officer  also  consulted  me  from  time  to  time 
for  some  months,  and  when  seen  always  had  a  pulse  of 
140,  and  there  was  every  reason  to  believe  that  this  rate 
was  maintained  in  the  intervals  between  his  visits  when  he 
went  about  as  usual.  He  was  gouty,  and  had  taken  wine 
and  spirits  very  freely.  Eventually  dropsy  set  in,  and  he 
died  from  heart  failure. 

In  Graves'  disease  a  permanent  rapid  pulse  is  one  of  the 
chief  characteristics  associated  with  enlargement  of  the 
thyroid,  exophthalmos,  etc. 

In  this  affection  the  tachycardia  is  attributed  by  most 
authors  to  excessive  secretion  by  the  thyroid  gland.  In 
favour  of  this  view  are  the  clinical  contrast  between  this 
disease  and  myxoedema,  the  increase  in  the  severity  of  the 
symptoms  when  thyroid  extract  is  administered,  and  the 
improvement  that  has  followed  in  some  cases  on  removal  of 
the  bulk  of  the  enlarged  thyroid. 

Others  consider  that  it  is  a  pure  neurosis,  as  the  exciting 
cause  can  frequently  be  traced  to  some  profound  shock  or 
emotional  disturbance. 

Paroxysmal  Tachycardia. — This  affection  is  characterized 
by  attacks  of  extreme  rapidity  of  the  heart's  action,  in 
which  the  pulse  rate  may  be  from  150  to  250  per  minute. 
The  attacks  may  last  some  days,  or  even  weeks.  They 
may  terminate  fatally  from  syncope,  or  cardiac  failure  and 
exhaustion,  or  may  suddenly  cease,  and  be  succeeded  by  a 
period   in   which   the   patient   enjoys   good    health.     They 


TACHYCARDIA.  395 

may  set  in  without  any  apparent  cause,  and  post-mortem  no 
gross  lesion  of  any  kind  is  found  in  the  valves  or  heart- 
muscle,  though  there  may  be  an  extreme  degree  of  dilatation 
of  the  heart  in  cases  in  which  the  tachycardia  has  persisted 
for  a  long  period. 

Bristowe,  quoted  by  Huchard,  gives  an  account  of  a 
remarkable  case  in  a  boy  aged  19  with  a  syphilitic  history, 
in  which  the  pulse  ranged  from  240  to  250,  then  became 
irregular,  with  periods  in  which  the  rate  was  200  for  10 
seconds,  alternating  with  others  in  which  it  fell  to  100. 
This  lasted  for  10  days,  when  the  pulse  suddenly  fell  to  60. 
Three  weeks  later  he  had  a  fresh  attack,  and  the  pulse  rate 
rose  to  288,  but  fell  to  84  when  he  took  to  his  bed.  A 
month  later  he  had  a  third  attack,  and  the  pulse  rate  rose 
to  308  when  he  was  up,  but  fell  to  64  when  he  lay  down. 
This  recurred  on  several  occasions,  and  fifteen  days  later 
he  died  suddenly  while  playing  the  piano. 

Pathogeny. 

The  main  cause  of  this  affection  must  be  some  derang-e- 
ment  of  the  nervous  mechanism  controlling  the  heart,  and 
opinions  are  divided  as  to  whether  it  may  be  due  to  ex- 
citation of  the  sympathetic  or  temporary  paralysis  of  the 
vagus,  or  to  some  affection  of  the  inhibitory  centre  in  the 
medulla.  There  is  little  to  be  said  in  favour  of  the  theory 
that  it  is  due  to  stimulation  of  accelerator  fibres  in  the 
sympathetic.  It  is  more  probable  that  it  may  be  due  to 
derangement  of  the  inhibitory  mechanism  in  the  medulla 
or  to  interference  with  inhibitory  impulses  descending  from 
this  centre  through  the  pneumogastric. 

There  is  no  evidence  in  support  of  bulbar  disease  as  a 
cause  of  tachycardia,  but  there  are  cases  on  record  in  which 
tachycardia  has  apparently  been  due  to  compression  of  the 
vagus  in  the  neck  by  enlarged  glands,  growths,  or  cicatricial 


396  HEART  DISEASE. 

tissue.  Instances  of  this  are  quoted  by  Huchard.*  In 
most  cases  of  tachycardia  gross  lesions  of  the  trunk  of  the 
vagus  can  be  excluded,  but  it  is  possible  that  its  fibres  may 
be  damaged  after  they  have  penetrated  the  myocardium, 
(a)  by  compression  in  cardiac  sclerosis  ;  (&)  by  spread  of 
inflammation  in  acute  myocarditis  ;  (c)  by  the  direct  action 
of  toxins  in  severe  toxaemias,  with  resulting  peripheral 
neuritis. 

There  is,  however,  no  definite  pathological  evidence  to 
support  this  surmise,  and  paroxysmal  tachycardia  is  not  a 
common  sequela  of  acute  toxaemias.  It  may  be  that  in- 
creased irritability  of  the  cardiac  muscle  is  the  more 
important  factor,  but  little  is  really  known  as  to  the 
pathogeny  of  this  obscure  affection. 

Tbeatment. 

In  tachycardia,  digitalis  and  the  cardiac  tonics  gene- 
rally, or  the  carminatives  which  are  useful  in  ordinary 
palpitation,  appear  to  have  little  or  no  influence  on  the 
frequency  of  the  heart's  action.  Rest,  mental  as  well  as 
bodily,  and  simple  diet  must  be  insisted  on,  and  any 
functional  derangements  of  the  abdominal  or  pelvic  viscera 
should  be  corrected.  The  drugs  which  have  seemed  to 
exercise  control  over  the  heart  have  been  bromides,  in  full 
doses,  and  belladonna  or  atropine,  pushed  to  the  limits  of 
tolerance. 

Huchard  has  found  digitalis  useful,  and  has  had  good 
results  in  three  cases  with  large  doses  of  quinine.  He  has 
also  given  ergotin  with  benefit. 

Thymus  gland  has  been  given  with  the  idea  that  it  is 
antagonistic  to  the  thyroid,  but  one  would  only  expect 
benefit  from  this,  if  at  all,  in  G-raves'  disease.  Galvanism 
of  the  vagi  has  been  tried,  and  sometimes  a  measure  of 
success  has  been  claimed  for  this  treatment. 
*  "  Mai.  du  Coeur,"  vol.  iii.  p.  866. 


TACHYCARDIA.  397 

Barr  *  states  that  lie  has  had  satisfactory  results  from 
the  administration  of  nitrite  of  amyl  and  nitroglycerine  in 
two  cases  of  paroxysmal  tachycardia.  It  will  be  seen  that 
drugs  of  a  widely  different  character  have  been  employed 
in  the  treatment  of  this  affection,  and  a  certain  measure  of 
success  has  been  claimed  for  each  in  individual  cases ;  but 
it  cannot  be  said  that  we  have  any  certain  means  of  reduc- 
ing the  rapid  action  of  the  heart,  and  a  certain  proportion 
of  cases  defy  all  known  methods  of  treatment. 

*  Barr,  "  Clin.  Lect.  on  Paroxysmal  Tachycardia,"  B.M.J.,  vol.  ii.  1U04, 
p.  109. 


CHAPTER   XXVII. 

DISORDERS  OF    RHYTHM  OF  THE   HEART 

{Continued). 

varieties  of  slow  pulse  and  their  causation — the 
condition  of  bradycardia  known  as  stokes- 
adams  disease — etiology — symptoms  —diagnosis  — 
prognosis — treatment. 

Varieties  of  Slow  Pulse  and  their  Causation. 

A  condition  of  permanent  slow  pulse  ranging  from  40  to 
60  may  be  hereditary  and  compatible  with  good  health. 
It  is  not,  however,  altogether  free  from  suspicion  of  liability 
to  heart  failure  under  the  stress  of  exertion  or  acute  illness. 
Pathologically,  it  may  be  associated  with  cerebral  tumour 
or  meningitis  (late  stages),  or  with  certain  conditions  of 
neurasthenia  and  with  melancholia. 

Extreme  slowness  of  pulse  is  also  met  with  sometimes 
in  toxic  conditions,  such  as  lead-poisoning,  when  it  may  be 
attributed  to  protracted  high  arterial  tension,  or  may  follow 
influenza,  diphtheria,  or  typhoid  fever,  the  toxins  of  which 
affect  the  integrity  of  the  cardiac  muscular  fibres.  It  may 
occasionally  supervene  in  uraemia,  and  in  jaundice  of  pro- 
longed duration.  Here,  again,  the  slowing  of  the  heart  is 
attributable  to  toxic  substances  in  the  blood.  It  has  been 
attributed  in  a  few  doubtful  cases  to  over-dosing  with 
digitalis  and  strophanthus  and  the  like.  This  affection  of 
slow  heart  action  is  to  be  differentiated  from  the  apparently 
slow  pulse  met  with  sometimes  in  cardiac  lesions,  in  which 


BRA  D  YCA  RDIA.  399 

the  pulse  seems  to  be  slow  because  all  the  heart-beats  are 
not  felt  as  a  pulse  at  the  wrist.  The  pulse  may  in  such 
cases  be  irregular,  as  well  as  infrequent,  but  cases  are  not 
uncommon  in  which  only  every  other  beat  reaches  the 
radial,  the  rate  at  the  heart  being,  say,  from  80  to  100, 
while  the  pulse  rate  as  counted  at  the  wrist  is  perfectly 
regular,  but  only  40  to  50. 

Stokes-Adams  Disease. 

In  addition  to  the  above  conditions  in  which  true  brady- 
cardia is  met  with  as  an  effect  of  various  recognizable 
influences,  there  is  a  certain  clinical  entity  characterized 
by  a  group  of  definite  symptoms  to  which  the  name  of 
Stokes-Adams  disease  has  been  given,  from  the  fact  that 
attention  was  first  called  to  it  by  Adams  in  1827,  while  it 
was  subsequently  described  in  fuller  detail  by  Stokes  in 
1836. 

The  disease  is  characterized  by  permanent  slow  pulse, 
ranging  habitually  as  low  as  20,  or  from  that  to  30  or  40, 
while  there  are  from  time  to  time  exacerbations  of  the 
infrequency  associated  with  syncopal,  epileptiform,  or 
pseudo-apoplectiform  attacks.  Sometimes  in  the  later 
stages  there  may  be  angina  pectoris  or  Cheyne- Stokes 
breathing. 

Etiology. 

The  condition  is  almost  invariably  associated  with  senile 
degenerative  changes  in  the  vascular  system.  The  patient 
is  usually  over  50  years  of  age,  and  the  artery  at  the  wrist 
is  large,  hard,  cord-like,  and  incompressible.  The  Avails  of 
the  vessel  are  thickened,  and  arterio-sclerosis  is  the  pro- 
minent feature.  Huchard,  quoted  by  Osier,  states  that  the 
etiology  of  the  condition  is  "  la  senilite  arterielle,"  *  and 

*  Lancet,  August  22,  1903. 


400  HEART  DISEASE. 

Osier  endorses  this  opinion,  although  he  gives  three 
instances  of  the  affection  in  young  subjects  in  the  interest- 
ing list  of  clinical  histories  of  cases  under  his  care. 

While  thickening  of  and  degenerative  changes  in  the 
vessels  are  constant  and  important  factors  in  the  Stokes- 
Adams  syndrome,  they  cannot  be  said  to  explain  the  brady- 
cardia or  other  phenomena. 

Huchard,*  commenting  on  the  frequency  of  arterio- 
sclerosis and  the  comparative  rarity  of  the  Stokes- Adams 
phenomena  in  association  with  it,  suggests  that  the  latter 
may  be  due  to  relative  angemia  of  the  medulla  from  athe- 
roma of  the  vessels  supplying  it.  In  support  of  this 
explanation,  he  refers  to  experiments  by  Brown-Sequard, 
Duret,  and  Conty,  showing  that  anEemia  of  the  bulb  causes 
slowing  of  the  pulse,  and  he  instances  the  slow  pulse  met 
with  in  certain  affections  of  the  nervous  system.  He 
considers  that  the  feeble  action  of  the  heart  may  be  a 
contributory  factor. 

Impairment  of  conductivity  of  the  muscular  fibres  between 
the  auricle  and  ventricle  has  been  suggested  by  Mac- 
kenzie of  Burnley  as  an  explanation  of  the  slow  pulse 
in  these  cases.  Gaskell  has  shown  that  in  the  frog's  heart, 
if  a  clamp  is  applied  along  the  auriculo-ventricular  groove, 
the  ventricle  can  be  made  to  respond  to  every  second,  third, 
or  fourth  contraction  of  the  auricle  or  to  remain  quiescent, 
according  to  the  tightness  of  the  clamp.  Mackenzie  f  calls 
attention  to  this,  and  has  demonstrated,  by  simultaneous 
tracings  of  the  auricular  wave  in  the  jugulars  and  the 
ventricular  pulse  in  the  carotids  and  radials,  that  similar 
phenomena  may  occur  in  the  human  heart.  He  has  shown 
that  in  a  case  of  slow  pulse  after  influenza  the  ventricle 
failed  to  respond  to  alternate  systoles  of  the  auricle,  and  in 
a  more  extreme  case  of  true  bradycardia  that  the  ventricle 

*  "  Mai.  du  Coeur,"  vol.  i.  p.  410. 
t  B.M.J.,  March,  1905. 


BRADYCARDIA.  401 

only  responded  to  every  third  auricular  systole.  He  there- 
fore attributes  the  slow  pulse  in  Stokes-Adams  disease  to 
blocking  of  conductivity  in  the  muscular  fibres  between  the 
auricle  and  ventricle.  According  to  my  experience,  there 
is  always  at  least  one  pulsation  in  the  jugulars  between  the 
beats  of  the  pulse. 

G-ibson  *  has  also  published  a  tracing  in  which  he  demon- 
strates four  auricular  beats  to  one  ventricular  in  a  case  of 
bradycardia,  and  he  also  attributes  the  phenomena  in  Stokes- 
Adams  disease  to  blocking  of  conductivity. 

Maynard  f  has  recently  published  an  interesting  case  of 
bradycardia,  in  which  he  noted  two  perceptible  impulses  of 
the  right  ventricle  associated  with  subsidiary  cardiac  sounds 
interpolated  between  the  beats  of  the  left  ventricle.  He 
concluded  that  these  sounds  and  impulses  were  produced 
in  the  right  side  of  the  heart  during  the  diastolic  pause  of 
the  left  ventricle.  This  gave  rise  to  some  criticism  by 
Gossage  and  Hay  as  to  whether  the  assumption  of  an 
independent  action  of  the  two  sides  of  the  heart  was  tenable. 
I  have,  however,  in  one  case,  seen  two  or  three  distinct 
right  ventricle  beats  interposed  between  each  systole  of  the 
left  ventricle.  The  beat  of  the  left  ventricle  came  at 
irregular  intervals  and  was  very  powerful,  giving  a  good 
radial  pulse,  but  it  did  not  always  exactly  coincide  with  a 
contraction  of  the  right  ventricle.  I  have  also  seen  cases 
in  which  an  independent  beat  of  the  right  ventricle  was 
present,  associated  with  a  pulsation  in  the  veins  of  the  neck, 
pointing  to  a  right  auricular  contraction  which  had  passed 
on  to  the  right  ventricle. 

Though  it  is  not  possible  to  demonstrate  the  contraction 
of  the  left  auricle,  I  think  we  may  assume  that  it  is  present 
in  these  cases,  but  is  not  transmitted  to  the  left  ventricle 
from  a  block   in   conductivity.      This  would    explain  the 

*  "  Nervous  Affections  of  the  Heart,"  1904.     (Fig.  23.) 
t  B.  M.J.,  vol.  ii.  1905,  pp.  847  et  seq. 

2d 


402 


HEART  DISEASE. 


absence  of  the  left  ventricle  beat,  and  would  not  entail  the 
assumption  of  independent  action  of  the  two  sides  of 
the  heart. 

The  left  ventricle  in  this  class  of  cases  is  usually  hyper- 
trophied  as  a  result  of  high  arterial  tension,  and  is  more 
subject  to  degenerative  changes,  and  it  is  conceivable  that 
it  would  require  a  more  forcible  stimulus  than  the  thinner 
walled  and  more  healthy  right  ventricle,  or  perhaps  a 
summation  of  stimuli,  to  throw  it  into  contraction. 

Symptoms. 
Of  the  symptoms,  the  syncopal  or  epileptiform  attacks 
are  the  most  frequent  and  the  most  striking.  They  are 
characterized  by  sudden  loss  of  consciousness  without  any 
warning,  in  which  the  patient  usually  falls  to  the  ground, 
as  in  an  epileptic  fit ;  but  there  are  very  rarely  general 
convulsions,  usually  only  slight  twitching  of  the  face  or 
extremities,  or  perhaps  none  at  all,  the  attack  resembling 
rather  that  of  petit  mal.  In  one  case  under  my  care  for 
two  years  (J.  F.  H.  B.)  the  patient  was  a  retired  colonel 
aged  74,  with  a  pulse  of  38  or  40,  who  had  from  time  to 
time  epileptiform  attacks  with  loss  of  consciousness  of  short 
duration,  in  which  he  fell  to  the  ground.  He  had  no  other 
symptoms,  no  dyspnoea  or  anginal  attacks,  and  up  to 
the  day  before  his  death  he  insisted  on  taking  a  daily 
promenade  in  the  street. 

The  epileptiform  attacks  are  accompanied  by  a  further 
fall  in  the  pulse  rate,  and  it  has  been  supposed  that  this 
was  a  consequence  of  the  seizures.  But  the  sudden  loss  of 
consciousness  and  convulsions,  when  they  occur,  are,  in  my 
judgment,  due  to  momentary  suspension  of  the  cerebral 
circulation  which  results  from  a  further  fall  in  the  pulse 
rate,  already  abnormally  slow. 

In  one  case  which  I  had  the  opportunity  of  observing, 
loss  of  consciousness  with  slight  twitching  of  the  face  took 


BRADYCARDIA.  403 

place  very  frequently,  and  occurred  on  more  than  one 
occasion  while  I  was  examining  the  heart.  Each  time  the 
heart-beat,  previously  very  slow,  was  suspended  for  a  long 
interval.  The  attack  then  came  on,  and  could  be  watched 
from  the  first.  If  in  the  act  of  speaking,  he  suddenly 
stopped,  the  expression  changed,  and  twitchings  of  the  face 
and  slight  general  movements  followed.  I  have,  however, 
seen  cases  in  which  there  was  well-marked  passive  dilatation 
of  the  stomach,  and  have  observed  a  diminished  tendency 
to  syncopal  and  epileptiform  attacks  when  this  condition 
was  treated  by  dieting  and  other  measures,  suggesting  that 
the  exciting  cause  of  the  syncopal  attacks  was  of  reflex 
gastric  origin. 

Diagnosis. 

The  slow  pulse  of  Stokes-Adams  disease  must  be  differ- 
entiated from  the  varieties  of  slow  pulse  enumerated  at  the 
beginning  of  this  chapter,  whether  physiological,  due  to 
toxic  substances  in  the  blood,  following  on  some  acute 
bacterial  infection,  or  associated  with  certain  diseases  of  the 
nervous  system. 

The  age  of  the  patient,  the  condition  of  the  vessels,  the 
occurrence  of  apoplectiform  and  epileptiform  attacks,  will 
usually  render  the  diagnosis  an  easy  matter.  The  epilepti- 
form attacks  can  be  distinguished  from  those  of  true 
epilepsy  by  their  association  with  the  slow  pulse  and  by  the 
previous  history  of  the  case.  The  fact  that  no  paralysis  or 
apparent  ill  effect  results  from  the  apoplectiform  seizures 
will  readily  mark  them  off  from  those  due  to  cerebral 
haemorrhage. 

Prognosis. 

This  is  necessarily  grave,  as  sudden  death  may  occur 
from  syncope,  from  angina  pectoris,  or  from  an  apoplecti- 
form   attack    followed   by    coma,    while    the    epileptiform 


404  HEART  DISEASE. 

seizures  involve  the  risk  of  an  accident  at  any  time.  As  a 
rule,  however,  it  does  not  prove  very  rapidly  fatal,  and 
patients  may  survive  for  many  months,  or  even  years. 

Tkeatment. 

The  condition  is  one  in  which  treatment  can  hardly 
be  expected  to  effect  any  great  improvement.  Iodide  of 
potassium,  nitroglycerine,  and  erythrol  tetranitrate,  which 
tend  to  keep  down  the  arterial  tension  and  make  the  work 
of  the  heart  easier,  are  often  of  great  service,  and  un- 
doubtedly tend  to  ward  off  the  epileptiform  and  apoplecti- 
form seizures. 

The  frequent  association  of  dilatation  of  the  stomach 
with  Bradycardia  must  be  borne  in  mind,  and  measures  for 
the  relief  of  this  condition  will  form  an  important  part  of 
the  treatment.  Recovery  may  take  place  even  when  Brady- 
cardia, indistinguishable  from  Stokes-Adams  disease,  has 
lasted  many  months,  and  appears  to  be  confirmed,  and 
cases  are  met  with  in  which  this' condition  comes  and  goes. 
Treatment  of  any  gastric  complication  should  therefore  be 
persevered  with,  and  careful  instructions  as  to  diet  should 
be  given. 

A  light  and  simple  diet  should  be  enjoined  in  all  cases, 
with  strict  moderation  in  animal  food,  if  it  is  taken  at  all. 
Hu chard  advises  a  strict  "regime  lacte,"  as  this  tends  to 
keep  the  arterial  tension  low  and  throws  least  work  on  the 
kidneys,  and  he  points  out  that  renal  inadequacy  is  common 
in  this  affection. 

A  certain  amount  of  gentle  exercise  may  be  taken  when 
it  is  well  borne  and  gives  rise  to  no  unfavourable  symp- 
toms, but  in  some  cases  the  slightest  effort  is  liable  to 
bring  on  a  cerebral  attack.  The  amount  of  exercise  which 
can  be  taken  must  be  decided  by  experience  in  each 
individual  case. 


CHAPTER  XXVIII. 

ACUTE  AORTITIS  OR  ACUTE  DEGENERATIVE 
LESIONS  OF  THE  AORTA. 

EXPERIMENTAL  EVIDENCE  —  ETIOLOGY—  MORBID  ANATOMY — 
PATHOGENY — PROGNOSIS — TREATMENT. 

Acute  aortitis,  in  its  typical  aspect,  as  described  by  Bizot, 
is  a  somewhat  rare  affection,  but  in  lesser  degrees  of  severity 
is  of  comparatively  frequent  occurrence,  and  has  not  received 
the  attention  it  deserves;  most  affections  of  the  aorta, 
even  in  acute  infections,  being  usually  loosely  classified  as 
"  atheroma."  Bizot,  in  1837,  and  Ranvier  in  1868,  gave  an 
account  of  the  pathological,  and  Bucquoy  and  Leger,  some 
years  later,  of  the  clinical  aspects  of  the  disease. 

Gilbert  and  Lion,  in  1889,  produced  acute  aortitis  experi- 
mentally in  rabbits  by  inoculation  of  micro-organisms  after 
first  injuring  the  aorta  with  a  stylet.  Boinet  and  Romary, 
in  1898,  succeeded  in  producing  acute  aortitis  experi- 
mentally by  inoculation  of  cultures,  and  also  of  the  toxins 
only,  of  various  micro-organisms,  which  in  some  instances 
attacked  the  wall  of  the  aorta  not  previously  injured  by  a 
stylet.  They  also  showed  that  degenerative  changes  set  in 
rapidly  in  the  affected  subendothelial  tissue.  They  further 
showed  that  the  administration  to  animals  for  some  months 
of  toxic  substances,  such  as  lead  and  uric  acid,  produced 
lesions  in  the  intima. 

Huchard,*  referring  to  their  experimeDts,  gives  a  remark- 

*  "  Maladies  du  Coeur,"  vol.  ii.  p.  270. 


406  HEART  DISEASE. 

able  illustration  by  Boinet  of  a  section  of  the  aorta  from 
a  case  of  facial  erysipelas,  in  which  typical  gelatiniform 
plaques  were  present  on  the  endothelium,  and  chains  of 
streptococci  were  seen  scattered  through  the  middle  coat. 

Mokbid  Anatomy. 

The  aorta  is  usually  dilated,  and  may  be  fusiform  or 
globular  in  shape.  On  laying  it  open  it  is  seen  to  be  of  a 
patchy  red  or  pinkish  colour,  and  the  surface  is  irregular 
and  uneven  for  a  distance  of  about  1^  to  2  inches  from  the 
aortic  valves.  The  uneven  surface  is  due  to  the  presence 
of  smooth,  pinkish,  rose-coloured,  or  greyish  patches  of 
varying  size,  termed  by  Bizot  "  gelatiniform,"  from  their 
opalescent  appearance.  The  colour  of  these  patches  may 
vary  from  a  pale  pink  or  grey  to  a  deep  red,  the  colouration 
being  mainly  due  to  post-mortem  staining  from  dissolved 
haemoglobin.  In  cases  of  less  severity  the  change  may  be 
limited  to  one  or  more  small  yellow  raised  opaque  patches, 
often  loosely  termed  atheroma. 

The  frontispiece,  drawn  from  a  recent  specimen  of 
primary  acute  aortitis,  well  shows  the  appearance  presented 
by  the  affected  aorta. 

On  microscopic  examination  of  these  gelatiniform 
plaques  or  patches,  the  endothelium  is  seen  to  be  swollen, 
and  beneath  it  are  necrotic  patches  infiltrated  with  flat, 
elongated  cells,  apparently  due  to  proliferation  of  the  con- 
nective tissue  elements.  The  middle  and  outer  coats  are 
less  affected,  but  they  may  be  swollen  and  infiltrated  with 
small  round  cells,  which,  in  the  adventitia,  are  chiefly 
conspicuous  round  the  vasa  vasorum. 

Etiology. 

Acute  Infectious  Diseases. — Acute  aortitis  may  occur  in 
the  course  of  scarlet  fever,  small  pox,  more  rarely  in  measles, 


ACUTE  AORTITIS.  4°7 

and  in  various  affections  of  known  bacterial  origin,  namely, 
typhoid  fever,  erysipelas,  pneumonia,  septicaemia,  influenza, 
rheumatism,  and  tuberculosis. 

In  young  children  who  have  died  of  pneumonia  or  septi- 
caemia, or  some  acute  bacterial  infection,  I  have  frequently 
seen  at  the  autopsy  small  yellow  raised  patches  in  the  aorta, 
which  may  be  regarded  as  instances  of  acute  degenerative 
lesions  due  to  the  action  of  micro-organisms  or  their  toxins. 

Acute  degenerative  lesions  of  the  aorta  may  also  occur 
in  severe  syphilis  in  the  secondary  stage,  and  also  in  gout 
and  lead  poisoning ;  but  in  these  affections  the  chronic? 
degenerative  change  known  as  atheroma  is  more  common, 
especially  in  tertiary  syphilis. 

Pathogeny. 

The  experimental  results  of  Gilbert  and  Lion,  and 
Boinet  and  Eomary,  referred  to  above,  throw  an  important 
light  on  the  pathogeny  of  acute  aortitis,  and  show  that  it  can 
be  produced  by  the  action  of  micro-organisms  and  their 
toxins. 

In  the  instances  in  which  the  vessel  wall  was  injured 
by  a  stylet,  one  must  presume  that  the  micro-organisms 
effected  their  entry  at  the  site  of  the  lesion  by  a  direct 
frontal  attack.  Where  acute  aortitis  resulted  from  inocula- 
tion without  previous  injury  to  the  vessel,  or  from  ingestion 
of  toxic  substances,  the  site  of  the  lesion  beneath  the 
intima,  and  the  cellular  infiltration  round  the  vasa 
vasorum  in  the  adventitia,  would  seem  to  indicate  that 
the  toxins  reached  the  affected  tissue  through  the  vasa 
vasorum.  The  immediate  result  appears  to  be  necrosis  of 
the  part  attacked,  as  there  are  areas  of  swollen  degenerated 
amorphous  tissue  beneath  the  intima.  Subsequently,  there 
is  an  attempt  at  repair  shown  by  the  presence  of  flattened 
proliferating  connective  tissue  cells.  As  the  vasa  vasorum 
normally  do  not  penetrate  the  middle  coat,  these  proliferating 


4o8  HEART  DISEASE. 

cells  are  not  vascularized,  so  there  is  no  formation  of 
fibrous  tissue  or  efficient  repair,  and  there  is  a  tendency  to 
the  deposition  of  lime  salts  in  the  affected  area.  In  many 
instances  of  so-called  atheroma  of  the  aorta,  as  will  be 
shown  later  in  the  chapter  on  that  affection,  we  find  vessels 
penetrating  the  media  and  extending  down  to  the  sub- 
endothelial  tissue,  which  may  be  an  attempt  to  vascularize 
newly  formed  connective  tissue  cells  proliferated  in  the 
process  of  repair. 

In  view  of  the  pathological  changes  found,  which  are 
of  the  nature  of  an  acute  necrosis,  the  term  acute  aortitis 
seems  scarcely  suitable,  and  I  would  suggest  "acute 
degenerative  lesions "  of  the  aorta  as  a  more  suitable 
nomenclature. 

Symptoms,  Physical  Signs,  and  Diagnosis. 

Throbbing  of  the  carotids,  a  sense  of  constriction  and 
burning  pain  behind  the  sternum,  a  feeling  of  intense 
oppression,  accompanied  by  paroxysms  of  dyspnoea,  have 
been  described  as  characteristic  features  of  this  affection. 
The  temperature  is  not,  as  a  rule,  raised,  except  as  a  result 
of  a  primary  infection  of  which  the  aortitis  may  be  a  com- 
plication. Dilatation  of  the  aorta  frequently  ensues,  but  as 
an  aorta  previously  dilated  from  atheromatous  degenera- 
tion may  be  attacked,  this  is  not  always  a  helpful  physical 
sign. 

Angina  pectoris  may  be  a  prominent  symptom,  as  the 
root  of  the  aorta  is  very  commonly  affected,  and  the  orifice 
of  one  of  both  coronary  arteries  may  be  obstructed  by  swell- 
ing of  the  adjacent  tissues. 

Huchard  attaches  considerable  importance  to  dilatation 
of  the  aorta,  and  considers  that  a  sudden  onset  of  severe 
symptoms  in  association  with  this  serve  to  render  a  diagnosis 
possible.     It  is,  however,  difficult  to  arrive  at  a  diagnosis 


ACUTE  AORTITIS.  409 

with  any  degree  of  certainty  during  life,  and,  in  the  absence 
of  angina,  it  can  rarely  be  made. 

An  interesting  account  of  two  cases  of  acute  aortitis  was 
published  in  the  Lancet  by  Poynton.*  One  of  these  cases, 
under  the  care  of  Dr.  Cheadle,  at  St.  Mary's  Hospital,  I 
had  the  opportunity  of  observing.  The  following  is  an 
account  of  the  case,  abridged  from  Dr.  Poynton's  description 
in  the  Lancet : — 

A  woman  aged  88  was  admitted  to  St.  Mary's  Hospital,  February, 
1899,  suffering  from  pain  in  the  heart  and  vomiting.  Two  months 
before  admission  she  had  suffered  from  attacks  of  precordial  pain 
extending  down  the  left  arm.  These  attacks,  infrequent  at  first,  had 
during  the  last  week  become  more  severe,  and  were  accompanied  by 
vomiting  and  faintness.  There  was  no  history  of  syphilis.  On  admis- 
sion she  was  well  nourished  and  free  from  pain,  but  shortly  after- 
wards she  had  an  attack  of  pain  in  the  left  arm,  with  a  feeling  of  faint- 
ness, which  Dr.  Cheadle  considered  to  be  true  angina  pectoris.  She 
volunteered  the  statement  that  any  sudden  exertion  was  liable  to  bring 
on  the  attacks  of  pain.  The  temperature  was  normal,  pulse  72,  but  at 
times  the  pulse  become  excited  and  irregular.  The  heart  was  not 
hypertrophied  ;  there  were  no  murmurs  at  the  base,  but  the  first 
sound  at  the  apex  was  sharp,  and  was  preceded  occasionally  by  a  short 
presystolic  murmur. 

At  midnight  three  days  after  admission  she  had  a  severe  attack  of 
angina  pectoris,  accompanied  by  vomiting,  and  she  died  two  hours 
later. 

At  the  autopsy  the  heart  was  slightly  dilated.  The  mitral  valve  was 
somewhat  thickened  from  old  endocarditis,  and  contained  a  calcareous 
nodule.  Its  orifice  was  slightly  stenosed.  Otherwise  the  heart  appeared 
to  be  normal. 

The  aorta  for  the  first  two  inches  was  extensively  diseased.  The 
intima  was  pinkish-red  in  colour,  with  raised  patches,  some  of  trans- 
lucent appearance,  others  yellow,  with  a  red  flush  round  their  bases. 
A  few  patches  resembled  the  condition  of  ordinary  atheroma.  The 
appearance  was  that  of  an  acute  aortitis,  supervening  on  a  more  chronic 
condition. 

This  is  well  shown  in  the  coloured  frontispiece,  which  was  drawn 
from  this  specimen. 

The  orifice  of  the  right  coronary  artery  was  slightly  narrowed,  but 
admitted  a  large  probe.     That  of  the  left  was  not  affected. 

Microscopical  Examination — 

Aorta. — The  intima  was  swollen.     The  vessels  were  distended,  and 

*  Lancet,  1809,  vol.  i.  p.  352. 


410  HEART  DISEASE. 

around  them  was  a  free  exudation  of  cells,  which  in  places  reached  the 
surface  of  the  intima.  The  elastic  coat  was  also  freely  infiltrated  with 
leucocytes.  Where  the  aorta  merged  into  the  heart- wall  the  exuda- 
tion could  be  traced  beneath  the  endocardium  of  the  left  ventricle. 

Heart  Muscle. — -This  showed  loss  of  striation,  extensive  hyaline,  and 
fatty  degeneration  in  many  places,  and  the  nuclei  showed  a  feeble 
staining  reaction.  In  some  places  between  the  muscle  fibres  there 
was  a  cellular  infiltration  and  an  appearance  of  active  reaction.  Some 
of  the  vessels  showed  an  increase  in  the  thickness  of  the  outer  coat,  but 
no  endarteritis  or  narrowing  of  their  lumen. 

Dr.  Poynton  points  out  that  there  was  no  disease  of  or  marked 
obstruction  of  the  orifices  of  the  coronary  arteries  to  explain  the 
anginal  attacks.  He  attaches  great  importance  to  the  profound 
changes  in  the  cardiac  muscle  accompanying  the  aortitis,  and  attri- 
butes death  to  cardiac  failure  from  this  cause. 


Prognosis. 

When  the  orifice  of  one  of  the  coronary  arteries  is  in- 
volved, and  attacks  of  angina  pectoris  result,  the  prognosis 
is  necessarily  very  grave. 

In  lesions  of  great  severity  affecting  the  arch  of  the 
aorta,  there  is  risk  of  sudden  death  from  perforation,  and 
recently  a  man  aged  46  was  brought  into  St.  Mary's 
Hospital,  moribund,  in  whom  a  post-mortem  examination 
disclosed  the  pericardium  full  of  blood,  and  a  minute  per- 
foration in  the  aorta  only  1  mm.  in  diameter,  the  result  of 
an  acute  degenerative  lesion. 

In  lesions  of  minor  severity  the  damaged  area  remains 
permanently  a  weak  spot,  and  may  later  on  in  life  give  rise 
to  an  aneurysm,  or  become  the  seat  of  a  calcareous  deposit. 

Treatment. 

If  the  affection  is  diagnosed,  absolute  rest  and  a  light 
non-nitrogenous  diet  should  be  enjoined.  For  the  attacks 
of  angina,  if  present,  nitrite  of  amyl  or  one  or  other  of  the 
nitrites  may  be  administered.  Iodide  of  potassium  and 
arsenic  may  be  given  with  advantage  as  the  attack 
subsides. 


CHAPTER  XXIX. 

ATHEROMA  OR  CHRONIC  DEGENERATIVE 
LESIONS  OF  THE  AORTA. 

ETIOLOGY    OF  GENERAL  ARTERIO-SCLEROSIS    AND    ATHEROMA 
—  MORBID    ANATOMY — PATHOGENY — DIFFERENT    VIEWS 
— PHYSICAL     SIGNS      AND      SYMPTOMS — AORTIC    INCOM- 
PETENCE    DUE     TO    DEGENERATIVE    CHANGE— ITS    DIS 
TINGUISHING    FEATURES — PROGNOSIS  —TREATMENT. 

Atheroma  of  the  aorta  is  a  degenerative  change  affecting 
primarily  the  deeper  layers  of  the  vessel  wall.  The  name 
is  derived  from  the  Greek  word  adapt]  or  adtipr\,  which  means 
"  gruel  "  or  "  porridge,"  and  emphasizes  the  fact  there  is 
softening  and  breaking  down  of  the  diseased  area. 

It  may  be  associated  with  degenerative  changes  affecting 
the  general  arterial  system,  commonly  termed  "  arterio- 
sclerosis," or  it  may  exist  independently  of  other  vascular 
lesions. 

Etiology. 

Atheroma  of  the  aorta  is  usually  a  disease  of  middle  or 
advanced  life.  Many  of  its  causes  are  the  same  as  those  of 
general  arterio-sclerosis,  which  comprise  : — 

1.  High  arterial  tension,  the  etiology  of  which  has  already 
been  discussed  in  Chap.  II.  Under  this  heading  we  have 
chronic  renal  disease,  gout,  over- eating  and  drinking, 
particularly  excessive  meat-eating,  associated  with  defective 
metabolism  and  imperfect  elimination. 

Heredity  plays  an  important  part,  more   especially   in 


412  HEART  DISEASE. 

association  with  the  last-mentioned  group  of  cases,  in  which 
the  tendency  to  early  vascular  degeneration  may  be  trans- 
mitted through  many  generations. 

2.  In  addition  to  high  arterial  tension,  which  involves  a 
constant  undue  strain  on  the  walls  of  the  whole  arterial 
system,  and  is,  as  has  already  been  said,  a  cause  of  general 
arterio-sclerosis,  there  is  one  form  of  intermittent  strain  con- 
nected with  certain  occupations,  which  affects  more  par- 
ticularly the  arch  of  the  aorta.  This  has  already  been 
referred  to  in  association  with  chronic  endocarditis  (p.  83). 
The  occupations  in  question  are  those  of  the  miner,  collier, 
gravedigger,  blacksmith,  and  hammerman,  which  involve 
violent  effort  in  a  constrained  and  cramped  position,  or 
exertion  during  which  there  is  prolonged  closure  of  the 
glottis  and  fixation  of  the  chest  in  holding  the  breath,  which 
give  rise  to  extreme  and  frequent  variations  in  the  blood 
pressure,  and  excessive  strain  on  the  walls  of  the  arch  of 
the  aorta.  Hence  dilatation  of  the  aorta  with  associated 
aortic  incompetence  are  particularly  liable  to  result 
General  arterio-sclerosis  is  usually  present  as  well  in  a 
marked  degree. 

3.  Lead  poisoning. 

4.  Diabetes  and  rheumatoid  arthritis  are  mentioned 
by  some  authors  as  causes  of  arterio-sclerosis.  In  diabetes 
in  young  subjects  I  have  frequently  seen  small  patches  of 
atheroma  in  the  aorta,  and  in  those  past  middle  life  exten- 
sive disease  of  the  cerebral  vessels,  but  in  most  instances  the 
diabetes  proves  fatal  before  any  extensive  general  arterio- 
sclerosis results.  In  rheumatoid  arthritis  and  chronic, 
joint  affections  thickening  and  hyperplasia  of  the  vessels 
are  frequently  met  with. 

5.  Alcohol  and  tobacco  are  usually  included  in  lists  of 
causes  of  arterio-sclerosis,  but  there  is  scarcely  sufficient 
evidence  to  prove  that  they  are  directly  responsible,  though 
the  wide  variations  of  blood  pressure  to  which  they  give 


ATHEROMA    OF  THE  AORTA.  413 

rise  must  have  a  deleterious  effect  apart  from  possible  toxic 
influences. 

Among  the  causes  of  atheroma  of  the  aorta  more  par- 
ticularly, as  apart  from  general  arterio- sclerosis,  are — 

1.  Syphilis. — This  is  one  of  the  most  important  causes  of 
degenerative  changes  in  the  aorta,  and  may  affect  the  aorta 
alone,  as  in  many  cases  of  aneurysm. 

2.  Bacterial  Infections. — These  have  already  been 
enumerated  and  their  modes  of  action  discussed  in  the 
chapter  on  acute  aortitis.  It  is  doubtful  how  far  they 
should  be  included  among  the  causes  of  chronic  degenera- 
tive change,  with  the  exception  of  tuberculosis,  and,  perhaps 
of  rheumatism,  but  it  is  difficult  to  draw  a  hard-and-fast  line 
between  acute  and  chronic  infections.  It  is  possible  that 
many  instances  of  so-called  atheroma  of  the  aorta  found  in 
later  life  may  be  the  result  of  an  acute  degenerative  lesion 
of  an  early  date,  in  which  calcification  or  imperfect  repair 
has  taken  place. 

Morbid  Anatomy. 

In  the  earlier  stages  the  inner  aspect  of  the  arch  of  the 
aorta  is  studded  with  opaque,  yellowish  elevations,  smooth 
on  the  surface,  and  varying  in  number,  size,  and  shape. 
Later  on,  ulceration  of  the  endothelial  surface  may  take 
place,  and  irregular  ragged  ulcers  result,  or  calcification  of 
the  diseased  areas  may  occur,  which  may  be  so  extensive 
that  a  portion  of  the  aorta  is  converted  into  a  rigid,  in- 
elastic, calcareous  tube. 

The  arch  of  the  aorta  is  most  commonly  affected,  but  the 
abdominal  aorta  may  be  attacked  as  well,  or  independently, 
or  the  whole  of  the  thoracic  and  abdominal  aorta  may  be 
diseased. 

Microscopic  Examination. — Microscopically,  in  a  section 
from  one  of  these  irregular  yellow  swellings,  the  endothelium 
is  seen  to  be  pushed   forward    by  a  mass  of  non-staining 


414 


HEART  DISEASE. 


necrotic  material,  in  which  may  be  distinguished  elongated, 

spindle-shaped  connective  tissue  cells  with  atrophic  small 
nuclei,  strands  of  swollen  fibrous  tissue,  and  in  the  deeper 
layers,  elastic  fibres  and  smooth  muscle  fibres,  the  latter 
undergoing  hyaline  degeneration.  (Vide  Fig.  25.)  In 
more  advanced  cases,  fat  droplets,  crystals  of  cholestrin, 
and  areas  of  calcification  may  be  present. 

The  degenerative  process  appears  to  start  in  the  intima 

^ :.     mBt&fcM M j)?w ■?>'•■•  ■ 

■   ',■•'.•. .-.. .  -      -    i-'j", ,;'-^y 


p), 


til 


mm 


FIG.    25. — SECTION   OF   WALL    OF    AOUTA,   SHOWING    EXTENSIVE    ATHEROMA 
AFFECTING    THE   MEDIA   AS   WELL   AS   THE   INTIMA. 

immediately  beneath  the  endothelium,  the  adjacent  layers  of 
the  media  being  next  affected,  or  sometimes  simultaneously. 

While  this  holds  good  for  arteries  of  lesser  size,  in  the 
aorta  the  seat  of  the  primary  degeneration  may  be  at  some 
point  in  the  deeper  layers  of  the  media,  particularly  in 
aneurysm,  as  will  be  pointed  out  later  in  the  chapter  on 
this  affection. 

The  vasa  vasorum  in  the  adventitia  are  usually  thickened, 


ATHEROMA    OF  THE  AORTA. 


415 


and  may  be  entirely  obliterated  in  places  as  the  result  of 
endarteritis,  as  in  Fig.  26,  taken  from  a  case  of  advanced 
atheroma  of  the  aorta  in  a  man  with  a  syphilitic  history. 
Sometimes  they  are  congested,  and  in  their  neighbourhood 
are  extensive  areas  of  round-celled  infiltration.  The  cells 
are  of  the  type  of  lymphocytes,  and  the  appearance  suggests 

■&  ■■         ■'    -''■■'- 

'■'  ',*'.<  if^'i     '>'"'<  -'w  ':;•  ^  v  -x  :. 
"ft;      /  -&  \&K  &&  x  V 


?W/.  '    >"'>« 


■-  •  :~Wr 


•'•" 


FIG.  2G. — SECTION  OF  ADVENTITIA  OF  THE  WALL  OF  THE  AORTA,  SHOWING 
ENDARTERITIS  OBLITERANS  OF  THE  VASA  VASORTJM.  A,  VESSEL  COM- 
PLETELY  OBLITERATED.       (X   80.) 

that  they  are  called  up  from  the  lymphatics  as  a  first  line 
of  defence  in  the  tissues  against  toxins  exuding  from  the 
vessels.  In  addition  to  these  lymphocytes,  there  may  be 
periarteritis  and  proliferation  of  connective  tissue  cells, 
which  is  the  second  line  of  defence  by  the  tissues.  Whereas, 
normally,  no  vessels  can  be  detected  in  the  middle  coat  of 
the  aorta,  frequently,  in  cases  of  atheroma,  numerous  small 


416  HEART  DISEASE. 

vessels,  offshoots  from  the  vasa  vasorum,  can  be  seen 
scattered  through  the  media,  penetrating  in  some  cases 
to  the  intima.  Sometimes  areas  of  round-celled  infiltration 
are  present  in  the  neighbourhood  of  these  vessels,  and  the 
middle  coat  is  extensively  disorganized  and  broken  up. 
(Vide  Fig.  21.) 


*~»<zi: 


FIG.    27. — SECTION    OP    MIDDLE    COAT    OF    AOKTA,   SHOWING    NUMEROUS    NEWLY 
FORMED   VESSELS. 

Pathogeny. 

Different  views  are  held  as  to  the  pathogeny  of  this 
condition.  Some  hold  that  the  primary  change  is  a  cell 
proliferation  in  the  sub-endothelial  connective  tissue,  as  a 
result  of  irritation  due  to  strain  or  some  toxic  material  in 
the  blood  stream,  and  that  subsequently  degeneration  of 
this  newly  formed  tissue  takes  place. 

Thoma  taught  that  the  thickening  of  the  intima  is  a 
secondary  or  compensatory  process  to  make  good  the  loss 
of  tissue  sustained  by  the  media. 

Neither  of  these  views  are  satisfactory.  On  micro- 
scopical examination  the  most  constant  feature  in  atheroma, 


ATHEROMA    OF  THE   AORTA.  4*7 

even  in  its  earliest  stages,  is  the  presence  of  amorphous, 
necrotic,  non- staining  materal.  The  attempt  at  cell  pro- 
liferation is  feeble,  and  one  never  sees  true  fibroblasts  with 
large  healthy  nuclei,  which  take  the  stain  well,  among  the 
newly-formed  cells  ;  the  nuclei  are  small  and  atrophic,  and 
the  half-starved  cells  seem  to  have  given  up  the  attempt  to 
form  new  fibrous  tissue. 

The  areas  of  atheromatous  tissue  do  not  always  fit 
into  depressions  in  the  media,  as  suggested  by  Thoma. 
In  the  section  of  the  atheromatous  coronary  artery  in 
Fig.  19,  p.  321,  it  will  be  seen  that  the  whole  of  the 
intima  is  extensively  diseased,  and  the  media  is  only 
affected  at  the  point  where  calcification  has  taken  place, 
that  is,  where  the  disease  in  the  intima  is  most  advanced.  In 
aneurysm  it  is  true  that  definite  atrophy  and  thinning  of 
the  media  and  a  depression  on  its  inner  aspect  can  be  made 
out.  Here  it  is  probable,  as  will  be  shown  later  in  the 
chapter  on  aneurysm,  that  focal  necrosis  in  the  inner  half 
of  the  media  may  be  the  primary  change,  but  the  condition 
is  different  to  that  which  obtains  in  atheroma  of  the  smaller 
vessels.  It  is  contrary  to  experience  that  nature  should 
attempt  to  repair  a  weak  spot  by  evolving  a  mass  of  useless 
necrotic  material,  which  is  what  is  suggested  by  those  who 
hold  that  the  atheromatous  tissue  is  compensatory  and 
secondary  to  degenerative  change  in  the  media. 

A  third  and  more  satisfactory  theory  is  that  the  primary 
change  is  a  degeneration  or  necrosis  of  the  sub- endothelial 
tissue  in  the  intima  and  deeper  layers  of  the  media.  This 
may  be  due,  among  other  causes,  to  the  cutting  off  of  nutri- 
ment by  obliterative  lesions  of  the  vasa  vasorum,  as  shown 
in  Fig.  26  in  the  case  of  syphilis. 

Huchard  *  attributes  all  forms  of  arterio- sclerosis  and 
atheroma  to  endarteritis  obliterans  of  the  vasa  vasorum,  and 
sums  up  his  conclusions  as  follows  : — 

*  "  Maladies  du  Cceur,"  vol.  i.  p.  163. 

2  E 


4i8  HEART  DISEASE. 

"  1.  Arteriosclerosis  or  atheroma  is  a  dystrophic  sclero- 
sis of  the  walls  of  the  vessels  consecutive  to  endarteritis 
obliterans  of  their  nutrient  arteries.  According  to  H. 
Martin,  atheroma  of  a  vessel  furnished  with  vasa  vasorum 
is  invariably  preceded  by  endarteritis  of  its  nutrient  vasa 
vasorum. 

"  2.  In  the  evolution  of  general  arterio-sclerosis  we  can 
distinguish  two  periods  anatomically :  (a)  development  of 
endarteritis  of  the  vasa  vasorum  ;  (b)  disorders  of  nutri- 
tion, which  are  a  consequence  of  this,  and  lead  to  general 
arterio-sclerosis  on  the  one  hand,  and  visceral  sclerosis  on 
the  other.  Clinically,  the  first  period  is  usually  latent,  but 
the  second,  that  of  disordered  nutrition,  gives  rise  to 
symptoms  more  or  less  distinctive." 

Huchard  *  meets  the  objection  that  the  vasa  vasorum 
cannot  be  traced  to  the  intima,  and  scarcely  even  penetrate 
the  media,  with  the  statement  that  it  is  for  this  very 
reason,  namely,  that  the  intima  is  most  distant  from  the 
source  of  nutriment,  that  the  degenerative  change  com- 
mences in  the  sub- endothelial  tissue  ;  the  endothelium 
itself,  being  nourished  by  the  general  blood  stream,  does 
not  usually  suffer. 

That  the  more  delicate  endothelium  of  the  vasa  vasorum 
may  be  affected  by  toxins  in  the  blood,  and  endarteritis 
result,  leading  to  obliteration  of  these  vessels  and  conse- 
quent atheroma  of  the  aorta,  is  shown  in  Fig.  26,  and  has 
already  been  demonstrated  by  Mott  t  in  the  case  of 
syphilis. 

It  is  possible  that  other  toxins  also,  e.g.  lead  and  uric 
acid  in  gouty  subjects,  may  act  in  the  same  way,  but  I  do 
not  think  that  obliteration  of  the  vasa  vasorum  is  invariably 
responsible  for  all  degenerative  lesions  of  the  aorta. 

It  is  probable  that,  in  some  cases,  the  areas  of  focal 

*  "Maladies  du  Cceur,"  vol.  i.  p.  158. 

t  Allbutt's  "  System  of  Medicine,"  vol.  vi.  p.  311. 


ATHEROMA    OF    THE  AORTA.  419 

necrosis  in  the  subendothelial  tissue  or  deeper  layers  of 
the  media  may  be  directly  due  to  the  destructive  action 
of  toxins  reaching  these  tissues  through  the  vasa  vasorum. 
These  toxins  may  be — 

(a)  Of  bacterial  origin. 

(b)  Metallic,  e.g.  lead. 

(c)  Antogenetic,  the  result  of  imperfect  metabolism,  as  in 
cases  of  high  arterial  tension  or  gout. 

The  explanation  of  the  presence  of  cellular  elements, 
which  have  the  appearance  of  atrophic  fibroblasts,  would 
seem  to  be  that  they  are  the  result  of  an  attempt  at  repair 
by  proliferation  of  connective  tissue  cells,  which  fails  because 
efficient  vascularization  cannot  take  place,  since  the  vasa 
vasorum  are  too  far  distant  to  throw  off  capillary  loops, 
which  would  have  to  traverse  the  media  before  they  reached 
the  newly  formed  tissue.  Thus  the  newly  formed  fibroblasts 
are  incapable  of  forming  new  fibrous  tissue,  and  themselves 
degenerate  in  turn, 

In  some  cases,  however,  numerous  vessels  can  be  seen 
penetrating  the  media  and  reaching  almost  down  to  the 
intima.  This  is  well  shown  in  Fig.  27.  Here,  I  take  it,  we 
have  an  attempt  at  vacularization  of  newly  formed  tissue  in 
the  media. 

This  could  scarcely  occur  if  the  primary  lesion,  causing 
focal  necrosis,  was  obliteration  of  the  vasa  vasorum,  but 
might  ensue  if  the  necrosis  was  an  acute  process  due  to  the 
destructive  action  of  toxins  conveyed  through  the  vasa 
vasorum,  and  was  followed  by  an  efficient  attempt  at  repair 
when  the  causative  toxaemia  had  subsided. 

Strain,  whether  intermittent  or  continuous,  is  an  im- 
portant etiological  factor  in  degenerative  lesions  of  the 
aorta,  more  especially  in  relation  to  aneurysm,  as  will  be 
seen  later. 

Conclusions. — Atheroma  is  a  focal  necrosis  of  the  sub- 
endothelial tissues  of  the  intima  or  the  adjacent  layers  of 


420  HEART  DISEASE. 

the  media,  due  either  to  the  destructive  actions  of  toxins 
conveyed  by  the  vasa  vasorum  or  to  loss  of  nutriment  from 
obliteration  of  the  vasa  vasorum  by  endarteritis. 

The  cellular  elements  are  the  result  of  an  attempt  at 
repair  by  proliferation  of  connective  tissue  cells,  which  fails 
because  efficient  vascularization  is  impossible. 

The  explanation  of  atheroma  due  to  intermittent  strain 
associated  with  arduous  occupations,  if  we  admit  that  strain 
alone  can  produce  atheroma,  may  be  that  it  is  in  part  due 
to  impaired  nutrition  of  the  deeper  layers  of  the  media, 
because  the  condition  of  over-tension  and  stretching  of  the 
aorta  interferes  with  the  passage  of  nutritive  fluids  through 
its  walls,  and  in  part  to  mere  mechanical  overstrain. 

Physical  Signs  and  Symptoms. 

Atheroma  of  the  aorta  in  its  early  stages  does  not  give 
rise  to  any  characteristic  physical  signs  or  symptoms.  The 
degenerative  process,  however,  is  commonly  not  confined  to 
the  aorta,  but  is  associated  with  general  arterio-sclerosis, 
evidence  of  which  will  be  found  in  the  thickened,  rigid, 
uneven  radials,  the  tortuous,  irregular,  and  prominent 
brachials,  which  are  thrown  into  curves  at  each  beat  of  the 
heart.  In  the  case  of  syphilis  and  acute  toxaemias,  the  aorta 
alone  may  be  affected.  The  aorta  frequently  becomes 
dilated  from  the  yielding  of  its  weakened  walls.  Some- 
times there  may  be  dulness  to  the  right  of  the  sternum,  and 
slight  pulsation,  but  this  is  seldom  apparent  except  in  the 
case  of  aneurysm  or  local  dilatation.  The  most  trustworthy 
sign  of  dilatation  is  the  alteration  in  the  character  of  the 
aortic  second  sound  as  heard  at  the  aortic  cartilage.  This 
becomes  low-pitched,  musical,  or  clanging  in  character,  and 
appears  to  be  prolonged. 

The  aortic  orifice  may  be  stretched  so  as  to  give  rise  to 
aortic  incompetence  from  imperfect  apposition  of  the  valves, 


ATHEROMA    OF  THE  AORTA.  421 

or  the  aortic  cusps  may  be  damaged  as  a  result  of  strain, 
and  be  involved  in  the  degenerative  process,  becoming 
thickened,  more  or  less  rigid,  and  incompetent. 

This  form  of  aortic  incompetence  differs  greatly  in  its 
characteristics  from  that  due  to  acute  endocarditis,  dis- 
cussed in  a  previous  chapter. 

Here  the  aortic  valves  have  become  incompetent,  usually 
as  a  result  of  high  arterial  tension  with  which  the  degenera- 
tive change  is  commonly  associated,  and  to  which  it  is 
secondary.  The  amount  of  regurgitation  is  slight ;  the 
diastolic  murmur  is  accompanied  by  a  low-pitched,  loud, 
ringing,  second  sound  ;  the  pulse  is  not  markedly  collapsing  ; 
the  artery  can  be  felt  between  the  beats,  and  is  usually 
thickened. 

The  arterial  tension,  though  somewhat  reduced,  remains 
high  in  spite  of  the  leakage,  because  the  abnormally  great 
peripheral  resistance,  the  original  cause  of  the  high  tension 
in  the  circulation,  is  unaltered,  and  the  heart  is  usually 
hypertrophied,  and  acting  powerfully.  Moreover,  in  this 
class  of  cases,  the  amount  of  regurgitation  is  seldom  very 
great.  I  have  found  the  blood  pressure,  estimated  by 
Riva  Rocci's  instrument,  to  range  from  140  mm.  to  190 
mm.,  as  contrasted  with  a  blood  pressure  of  90  to  120  mm. 
in  cases  of  aortic  regurgitation  due  to  acute  endocarditis, 
in  which,  for  reasons  given  in  Chapter  II.,  the  mean  blood 
pressure  is  usually  low. 

It  is  the  indiscriminate  classification  of  cases  of  aortic 
incompetence  in  which  the  valves  have  given  out  as  a  result 
of  strain  and  high  arterial  tension,  with  the  totally  different 
group  in  which  the  valves  have  been  rendered  incompetent 
by  acute  endocarditis,  and  to  a  great  extent  destroyed, 
that  has  given  rise  to  so  much  discrepancy  of  opinion 
as  to  the  mean  blood  pressure  or  arterial  tension  in  aortic 
regurgitation. 

Aneurysm. — One  of  the  most  serious  results  of  atheroma 


422  HEART  DISEASE. 

of  the  aorta  is  local  weakening  of  its  wall,  which  may  lead  to 
the  formation  of  an  aneurysm. 

Occlusion  of  Coronary  Arteries. — Atheromatous  change  in 
the  neighbourhood  of  the  orifices  of  the  coronary  arteries 
may  partially  occlude  one  or  both  of  them,  and  give  rise  to 
angina  pectoris,  or  to  fibroid  change  in  the  heart  wall. 

Prognosis. 

Inasmuch  as  atheroma  is  a  degenerative  change,  is 
usually  progressive,  and  may  give  rise  to  aneurysm,  dilata- 
tion of  the  aorta,  aortic  incompetence,  and  impair  the  nutri- 
tion of  the  heart  by  occlusion  of  the  coronary  vessels,  the 
prognosis  is  necessarily  grave.  As  regards  the  duration  of 
life,  much  will  depend  on  the  nature  of  the  secondary 
change  in  the  aorta  to  which  the  atheroma  gives  rise,  and 
on  the  influences  to  which  the  patient  is  exposed. 

Treatment. 

When  atheroma  of  the  aorta  is  associated  with  general 
arterio-sclerosis  and  high  arterial  tension,  as  is  most  com- 
monly the  case,  treatment  must  be  directed  to  lowering  the 
latter,  so  that  a  minimum  amount  of  strain  may  be  thrown 
on  the  great  vessels  and  heart. 

Alcohol,  tobacco,  stimulants  of  all  kinds,  should  be  for- 
bidden. Strict  moderation  in  diet  should  be  enjoined,  and 
meat,  game,  and  soups  should  be  eschewed  as  far  as  possible. 
In  some  cases  a  strict  milk  diet  may  be  advisable  for  a  time. 
Undue  exertion  and  excitement  should,  as  far  as  possible,  be 
avoided,  but  gentle  walking  exercise  may  be  taken.  Mild 
mercurial  purgatives  should  be  given  once  or  twice  a  week, 
and  these  may  be  supplemented,  if  necessary,  by  a  morning 
draught  of  a  sulphated  mineral  water  such  as  Hunyadi, 
Janos,  Apenta,  Friedrichshall,  and  the  like. 

Vaso-dilators,  trinitrin,  or  erythrol   tetranitrate  should 


ATHEROMA    OF  THE  AORTA.  423 

be  administered  if  the  blood  pressure  is  high,  as  they  tend 
to  lower  the  arterial  tension  by  diminishing  the  peripheral 
resistance.  Iodide  of  potassium  may  be  given  in  addition, 
often  with  marked  benefit. 

When  there  is  reason  to  believe  that  the  degenerative 
change  in  the  aorta  is  the  result  of  syphilis,  iodide  of 
potassium  should  be  freely  administered  for  a  long  period, 
either  alone  or  in  combination  with  mercury. 


CHAPTEE  XXX. 
ANEUEYSM  OF  THE  AECH  OF  THE  AOETA. 

MORBID  ANATOMY  —  ETIOLOGY  —  PATHOGENY  —  RELATIONS 
OP  THE  AECH  OF  THE  AOETA — PHYSICAL  SIGNS  AND 
SYMPTOMS — ANEURYSM  (1)  OF  THE  INTEA-PEEICAEDIAL 
POETION  OF  AOETA  ;  (2)  OF  ASCENDING  AOETA  ;  (3)  OF 
TRANSVERSE  PART  OF  ARCH  ;  (4)  OF  DESCENDING  AORTA 
— DIAGNOSIS — PROGNOSIS — TREATMENT. 

An  aneurysm  is  a  pulsating  tumour  in  connection  with 
the  interior  of  an  artery.  It  is  caused  by  the  bulging  or 
giving  way,  under  the  blood  pressure  of  a  portion  of  the 
wall  of  an  artery  weakened  by  injury  or  disease.  It  may  be 
saccular,  fusiform,  or  cylindrical  in  shape,  according  to  the 
extent  and  area  of  the  arterial  wall  which  gives  way  in 
the  first  instance. 

Morbid  Anatomy. 

A  cylindrical  or  fusiform  aneurysm  is  merely  a  general 
dilatation  of  the  vessel  in  some  part  of  its  course. 

A  saccular  aneurysm  is  caused  by  the  giving  way  of  a 
circumscribed  portion  of  the  vessel  wall  as  the  result  of 
some  morbid  process  affecting  the  deeper  layers  of  the 
media.  This  weak  spot  gradually  bulges  and  yields  more 
and  more  under  the  blood  pressure.  The  dilated  portion  is 
termed  the  sac,  and  the  orifice  by  which  it  communicates 
with  the  interior  of  the  vessel  is  termed  the  mouth  of  the  sac. 

The  intima  can  usually  be  traced  for  a  varying  distance 
on  to  the  interior  of  the  sac. 


ANEURYSM  OF  THE  ARCH  OF  THE  AORTA.  425 

The  media  is  greatly  thinned  ;  the  muscular  fibres  are 
atrophied  and  compressed,  and  have,  to  a  great  extent, 
disappeared ;  the  elastic  fibres  are  stretched  and  have  lost 
their  elasticity,  and  may  be  rnptured  in  places.  The 
adventitia  is  thickened  from  formation  of  new  fibrous  tissue, 
so  that  the  wall  of  the  sac  consists  mainly  of  the  thickened 
adventitia,  with  which  may  be  incorporated  adjacent  struc- 
tures to  which  it  becomes  adherent. 

As  the  aneurysm  increases  in  size  and  the  mouth  of  the 
sac  becomes  relatively  small  in  comparison  with  its  interior, 
the  circulation  of  blood  in  the  sac  becomes  sluggish, 
and  layers  of  laminated  clot  are  deposited  on  the  diseased 
walls. 

The  so-called  dissecting  aneurysm  is  not,  strictly 
speaking,  a  true  aneurysm.  In  this  condition  there  is  a 
rupture  of  the  intima  and  of  a  portion  of  the  media,  through 
which  the  blood  penetrates  the  media  and  tears  its  way 
downwards  in  its  substance  for  a  varying  distance,  some- 
times finding  its  way  back  again  into  the  interior  of  the 
vessel  at  a  lower  level. 


Etiology. 

Age. — Aneurysm  is  a  disease  of  middle  and  advanced 
life,  but  is  met  with  also  in  young  adults. 

Sex  and  Occupation. — It  is  far  more  common  in  men  than 
in  women,  which  seems  to  point  to  hard  work  and  laborious 
occupations  as  a  factor  in  its  production.  It  is  frequently 
met  with  in  soldiers  and  miners  ;  the  prolonged  and  severe 
exertion  to  which  the  former  are  subjected  in  campaigning 
and  forced  marches,  together  with  the  restraint  on  the  free 
play  of  the  chest  wall  by  arms  and  accoutrements,  the 
arduous  nature  of  the  work  of  the  latter,  and  the  constrained 
and  cramped  position  in  which  they  have  to  work,  have  been 


426  HEART  DISEASE. 

held  to  account  for  its  common  occurrence  in  men  following 
these  occupations. 

Atheroma  of  the  aorta,  a  comprehensive  term,  in  ordinary 
parlance,  for  degenerative  lesions  of  the  aorta,  of  whatsoever 
origin,  is  one  of  the  commonest  causes  of  aneurysm.  Its 
etiology  has  already  been  discussed  in  the  last  chapter,  but 
as  extensive  and  widespread  atheroma  of  the  aorta  is  of 
common  occurrence  without  aneurysm,  it  is  clear  that 
certain  factors  must  be  more  particularly  concerned  in  the 
production  of  the  latter.     These  are — 

I.  Affections  which  give  rise  to  circumscribed  or  focal, 
rather  than  general,  lesions  of  the  aorta. 

II.  Conditions  of  varying  and  high  blood  pressure 
within  the  aorta. 

Among  the  former  are — 

(a)  Syphilis. — This  is  unquestionably  one  of  the  most 
important  factors  in  the  production  of  aneurysm,  and  about 
this  opinion  is  almost  unanimous.  Welsh  found  a  history 
of  syphilis  in  50  per  cent.,  Frankel  in  47  per  cent.,  and 
Huchard  in  43  per  cent,  of  cases  of  aneurysm  of  the  aorta. 
Drummond  of  Newcastle  considered  that  in  a  large  pro- 
portion of  cases  of  aneurysm  in  miners,  attributed  to  strain, 
syphilis  was  mainly  responsible,  and  this  may  be  so,  in 
soldiers,  in  whom,  also,  syphilis  is  very  common. 

It  seems  probable  that  syphilis  may  produce  focal  lesions 
of  the  aorta  in  two  ways  — 

(1)  In  the  secondary  stage  by  a  toxic  action  on  the 
vessel  wall  similar  to  that  of  acute  bacterial  infections. 

(2)  In  the  later  stages,  by  setting  up  endarteritis  obli- 
terans of  the  vasa  vasorum  of  the  aorta,  at  one  or  more 
points,  and  thus  depriving  its  wall  of  the  necessary  nutri- 
ment, with  resulting  slow  necrosis  and  degenerative  change 
in  the  deeper  layers  of  the  media  in  corresponding  circum- 
scribed areas. 

(b)  Acute  Bacterial  Infections.— These  I  would  suggest 


ANEURYSM  OF  THE  ARCH  OF  THE  AORTA.  427 

as  causes  next  in  importance  to  syphilis.  I  am  aware  that 
they  are  not  generally  recognized  etiological  factors,  but 
the  experimental  results  of  Boinet  and  Romary,  detailed  in 
Chapter  XXVIII.,  afford  strong  support  to  this  view,  which 
has  also  certain  pathological  evidence  in  its  favour.  As 
already  explained,  it  is  probable  that  the  toxins  evolved  by 
the  micro-organisms  reaching  the  aorta  through  the  vasa 
vasorum  give  rise  to  areas  of  focal  necrosis  in  the  deeper 
layers  of  the  media.  Efficient  repair  does  not  take  place, 
and  a  weak  spot  in  the  vessel  wall  results,  which  in  later 
life,  possibly  some  years  after  the  primary  lesion,  when 
other  factors  have  given  rise  to  high  arterial  tension  and 
increased  blood  pressure  in  the  aorta,  may  become  the  site 
of  an  aneurysm. 

Huchard  *  holds  that  whereas  gout,  atheroma,  syphilis, 
alcoholism,  and  malaria,  which  may  set  up  focal  degenera- 
tion in  the  media,  are  predisposing  causes,  the  supervention 
of  some  acute  bacterial  infection  is  commonly  the  immediate 
cause  of  aneurysm.  In  support  of  this,  he  instances  the 
development  of  an  aneurysm  in  syphilitic  and  gouty  sub- 
jects, which  he  has  observed  subsequent  to  a  severe  attack 
of  influenza. 

(c)  Toxins  other  than  Bacterial. — Lead  poisoning,  which 

is  a  common  cause  of  general  arterio- sclerosis,  can  seldom 

be  traced  as  a  factor  in  aneurysm.     We  have  little  direct 

evidence  as  to  the  part  played  in  the  production  of  aneurysm 

by  alcohol,  or   organic  poisons  such   as  may  result  from 

imperfect    metabolism    in    gouty    and    plethoric   subjects. 

Fischer  f   of   Bonn   has,   however,    recently   published   an 

account  of  experiments  in  which  he  was  able  to  produce 

aneurysms  in  rabbits  by  repeated  injections  of  adrenalin 

or  digalen,  and  in   the  light  of  these  it  is  possible  that 

a  variety  of  toxins  may  be  etiological  factors  in  aneurysm. 

*  "  Mai.  du  Cceur."  vol.  ii.  pp.  372,  373. 

t  Dent.  Med.  Woch.,  October  26,  190.5,  pp.  1713  et  seq. 


42S  HEART  DISEASE. 

These  experiments  will  be  referred  to  in  more  detail 
later  on. 

Gkoup  II.  Varying  Conditions  of  High  Blood  Pressure  in 
the  Aorta. — The  strain  to  which  the  walls  of  the  arch  of 
the  aorta  are  subjected  by  the  varying  conditions  of  the 
blood  pressure  within  is  greater  than  in  any  other  vessel. 

The  blood,  as  it  is  forcibly  expelled  from  the  ventricle  at 
each  systole,  rapidly  expands  the  aorta,  and  impinges  on 
the  dome  of  the  arch  by  which  it  is  deflected.  The  respira- 
tory variations  of  the  blood  pressure  are  also  very  consider- 
able. The  pressure  is  raised  in  inspiration,  and  in  occupa- 
tions which  involve  severe  effort  in  cramped  positions, 
frequently  with  the  glottis  closed,  the  strain  imposed  on 
the  walls  of  the  arch  must  be  greatly  increased.  Strain  on 
the  vessel  wall,  more  especially  intermittent  strain  due  to 
fluctuations  in  the  blood  pressure,  which  occur  in  these 
arduous  occupations,  such  as  those  of  the  miner,  collier, 
soldier,  is  unquestionably  an  important  etiological  factor  in 
aneurysm. 

I  have  seen  two  cases  of  spontaneous  rupture  of  the 
intrapericardial  portion  of  the  aorta  in  which  there  was  no 
patch  of  atheroma  or  indication  of  previous  disease.  The 
aorta  was  greatly  dilated  and  stretched  in  both  instances, 
and  its  walls  were  about  the  thickness  of  ordinary  brown 
paper.  One  was  in  a  man  aged  42,  who  was  brought  in 
dead  to  St.  Mary's  Hospital ;  the  other  was  in  a  boy  aged  20, 
with  pneumothorax  on  the  left  side.  The  rupture  in  this 
case  occurred  when  the  boy  was  apparently  convalescent, 
three  months  after  the  onset  of  the  pneumothorax. 

Pathogeny. 

The  interesting  paper  of  Fischer  of  Bonn  already  re- 
ferred to  throws  much  light  on  the  pathogeny  of  aneurysm. 
He  describes  how  he  has  been  able  to  produce  aneurysm 


ANEURYSM  OF  THE  ARCH  OF  THE   AORTA.  429 

of  the  aorta  in  rabbits  experimentally  by  repeated  injections 
of  adrenalin. 

Josue  had  previously  produced  arterio-sclerosis  and 
atheroma  in  rabbits  by  injections  of  adrenalin,  and  his 
results  have  been  confirmed  by  other  investigators,  includ- 
ing Fischer,  who  describes  his  results  with  adrenalin  as 
follows : — 

"  The  first  alterations  are  circumscribed  areas  of  necrosis 
of  the  smooth  muscle  fibres  of  the  media.  Dilatation  of  the 
aorta  with  straightening  out  of  the  elastic  fibres,  which 
normally  have  a  wavy  outline,  is  the  next  change.  The 
thick  elastic  lamella?  are  approximated,  and  the  more 
delicate  elastic  fibres  between  them  disappear.  In  most 
cases  calcification  of  the  necrotic  area  sets  in  early,  so  that 
a  compact  lamina  of  lime  salts  is  found  in  the  media,  and 
the  elastic  fibres  in  the  neighbourhood  are  torn  and 
destroyed.  I  have  thus  demonstrated  that  this  process 
differs  materially  from  human  arterio-sclerosis,  and  that  a 
primary  necrosis  of  the  muscular  fibres  and  the  elastic 
lamella?  of  the  media  is  the  cause  of  it.  I  have  therefore 
given  to  this  condition  the  name  '  arterio-necrosis.'  " 

Fischer  has  also  shown  that  various  toxic  substances 
besides  adrenalin  can  produce  this  condition  of  arterio- 
necrosis  in  rabbits,  but  not  aneurysm,  which  apparently 
requires,  in  addition,  the  increased  blood  pressure  induced 
by  the  administration  of  adrenalin.  He  has  produced  a 
typical  aneurysm  of  the  aorta  in  a  rabbit  by  twenty-one 
intravenous  injections  of  adrenalin  (1  in  1000),  in  doses  of 
0*3  to  0*5  ccm.,  and  in  one  instance,  a  dissecting  aneurysm  of 
the  aorta  after  twenty-three  similar  injections  of  adrenalin. 
He  has  also  succeeded  in  producing  aneurysm  by  repeated 
injections  of  digalen,  a  preparation  of  digitalis  which  would 
have  similar  effect  to  adrenalin  in  raising  the  blood  pressure. 
He  found  that  the  arch  of  the  aorta  was  most  commonly 
affected  first,  and  next  in  sequence,  the  thoracic  aorta. 


43o  HEART  DISEASE. 

This  experimental  evidence  would  seem  to  point  to  a 
focal  lesion  of  the  deeper  layers  of  the  middle  coat  of  the 
aorta  as  the  primary  lesion  or  predisposing  cause,  and  to 
undue  increase  of  the  blood  pressure  within  its  walls  as  the 
exciting  cause  of  aneurysm. 

It  is  remarkable  that  in  chronic  interstitial  nephritis,  in 
which  the  blood  pressure  is  higher,  perhaps,  than  in  any 
other  affection,  aneurysm  is  comparatively  rare.  The  ex- 
planation of  this  would  seem  to  be  (1)  that,  as  the  rise  in 
blood  pressure  is  gradual,  the  vascular  system  has  time  to 
adapt  itself  to  the  increased  strain  by  hypertrophy  of  its 
muscular  coat,  and  is,  moreover,  maintained  in  a  condition 
of  hypertonus  ;  (2)  that  the  disease  does  not  tend  to  produce 
a  focal  lesion  in  the  aorta.  Mac  William*  has  demonstrated 
that  in  contracted  arteries,  the  range  of  pulsatile  expansion 
is  much  less  than  in  relaxed  vessels,  and  that  there  is  a 
greater  tendency  to  elongation  and  tortuosity,  and  con- 
sequently to  dilatation  of  relaxed  vessels  subjected  to  strain. 
The  maintenance  of  a  condition  of  hypertonus  is  therefore 
protective  against  aneurysm. 

In  the  arduous  occupations  which  have  been  referred  to 
above  as  predisposing  to  aneurysm,  there  is  no  protective 
hypertonus  of  the  vessels ;  the  strain  is  intermittent,  and 
not  constant,  and  may  take  place  when  the  aorta  is  relaxed 
and  more  or  less  defenceless,  so  that  the  conditions  are 
more  favourable  to  aneurysm.  It  is,  however,  doubtful 
if  this  can  result  from  strain  alone,  in  the  absence  of 
a  previous  focal  lesion  of  the  vessel  wall.  The  impor- 
tance of  a  focal  lesion  as  a  factor  in  aneurysm  is  clearly 
demonstrated  in  syphilitic  lesions  of  the  aorta,  in  which 
no  rise  of  blood  pressure  above  the  normal  appears  to 
be  necessary  to  dilate  the  weakened  area  and  give  rise 
to  aneurysm. 

*  Properties  of   Arterial  and  Venous  Walls,  Proc.  Boy.  Soc,  vol.  lxx. 
p.  151. 


ANEURYSM  OF  THE   ARCH  OF   THE   AORTA.  431 


Anatomical  Belations  of  the  Arch  of  the  Aorta. 

Before  discussing  the  physical  signs  of  aneurysm,  we 
must  call  to  mind  the  'position  and  chief  relations  of  the  arch 
of  the  aorta,  as  many  of  the  symptoms  and  physical  signs 
of  aneurysm  are  directly  dependent  on  pressure  effects  of 
the  dilated  portion  of  the  vessel  on  the  adjacent  structures. 

The  aorta,  as  it  emerges  from  the  left  ventricle  behind 
the  pulmonary  artery,  and  overlapped  by  the  appendix  of 
the  right  auricle,  takes  an  oblique  course  upwards,  to  the 
right  and  forwards,  to  the  level  of  the  upper  border  of  the 
second  right  costal  cartilage  ;  this,  anatomically,  is  termed 
the  ascending  aorta,  but  in  discussing  aneurysm  it  will  be 
more  convenient,  clinically,  to  include  under  this  head,  the 
portion  of  the  aorta  from  the  pericardium  to  the  origin  of 
the  innominate.  The  most  important  relations  of  the 
ascending  portion  of  the  arch  with  reference  to  the  symptoms 
to  which  aneurysm  of  this  part  may  give  rise,  are,  the  vena 
cava  superior  on  the  right  or  outer  side,  and  the  root  of  the 
right  lung  posteriorly ;  but,  as  there  is  free  and  extensive 
movement  of  this  portion  of  the  aorta  at  each  cardiac  systole, 
and  provision  is  made  for  this,  the  surrounding  structures 
are  not  in  very  close  relation  to  the  vessel :  hence  pressure 
symptoms  will  not  arise  till  the  aneurysm  has  attained  a 
considerable  size.  It  must  not  be  forgotten  that  part  of 
the  aorta  lies  free  in  the  pericardial  cavity  for  a  short 
distance  from  its  origin  ;  aneurysms  of  this  intra-pericardial 
portion,  more  especially  of  one  of  the  sinuses  of  Valsalva, 
are  liable  to  rupture  and  cause  sudden  death  before  any 
physical  signs  or  symptoms  arise  which  would  lead  one 
to  suspect  their  presence. 

The  second  or  transverse  part  of  the  arch  of  the  aorta 
has  a  direction  backward  and  to  the  left,  and  comprises  the 
portion  of  the  vessel  between,  and  including  the  orifices  of 


432 


HEART  DISEASE. 


the  innominate  and  left  snb-clavian  arteries.  This  portion 
has  little  freedom  of  movement,  and  lies  in  close  relation  to 
several  important  structures,  pressure  on  which  may  early 

rl'hyroid  gland 


Right  vagu 

Re.c  u  rrent 


Left  vayiis 
-Left  phrenic 
Ihoracic  aurt 


fig.  28. — relations  of  akcu  of  aorta.     From  Gray's  Anatomy. 

give  rise  to   characteristic   symptoms.     Behind  it  lie  the 
trachea,  oesophagus  and  thoracic  duct :  interposed  between 


ANEURYSM  OF  THE  ARCH   OF  THE  AORTA.  433 

it  and  the  trachea  just  above  the  bifurcation  is  the  deep 
cardiac  plexus ;  the  left  recurrent  laryngeal  nerve  also 
curves  round  it  and  ascends  towards  the  trachea  on 
its  posterior  surface.  In  front  the  left  vagus  and  left 
phrenic  nerves  and  the  two  superficial  cardiac  nerves  from 
the  sympathetic  and  pneumogastric  respectively,  cross  its 
anterior  surface  which,  from  its  oblique  course,  looks  to  the 
left  as  well  as  forwards.  Above  is  the  left  innominate 
vein ;  from  its  upper  aspect  are  given  off  the  innominate 
and  left  carotid  and  sub-clavian  trunks.  Below  is  the 
bifurcation  of  the  pulmonary  artery,  the  left  bronchus,  and 
the  left  recurrent  laryngeal  nerve  as  it  winds  round  the  aorta. 

The  third  or  descending  part  of  the  arch  completes  the 
curve  downward  and  backward.  It  descends  behind  the  root 
of  the  left  lung  to  lie  to  the  left  of  the  body  of  the  fourth 
dorsal  vertebra. 

As  has  been  shown  in  the  brief  sketch  of  the  course 
and  relations  of  the  arch  of  the  aorta,  the  ascending  portion 
is  near  the  surface  of  the  chest  and  accessible  to  physical 
examination,  has  no  attachments  to  surrounding  structures, 
and  enjoys  considerable  freedom  of  movement.  Aneurysm 
here  often  attains  to  considerable  size  before  it  begins  to 
give  rise  to  any  symptoms  from  pressure  on  surrounding 
organs,  so  that  the  first  indication  of  its  presence  may  be 
a  pulsating  tumour  visible  on  the  chest  wall  to  the  right 
of  the  manubrium. 

The  transverse  portion  of  the  arch,  on  the  contrary,  is 
deeply  placed,  is  more  or  less  firmly  fixed  in  position,  and 
is  in  such  close  relation  to  various  important  structures,  that  a 
projection  from  its  surface  cannot  elude  or  be  eluded  by  the 
surrounding  parts.  Hence  aneurysm  of  this  portion  of  the 
aorta  before  it  attains  any  great  size,  usually  gives  rise 
to  symptoms  from  pressure  on  adjacent  structures,  of  which 
a  brassy  cough  and  cracked  voice,  or  tracheal  breathing 
.and  difGculty  of  deglutition,  may  be  the  indications. 

2  F 


434  HEART  DISEASE. 

I  have  consequently  been  led  to  divide  thoracic  aneu- 
rysms into  two  classes,  namely  Aneurysms  of  Physical  Signs 
and  Aneurysms  of  Symptoms,  from  the  predominance  of 
physical  signs  and  symptoms  respectively,  the  former 
term  applying  to  aneurysms  of  the  ascending  aorta  and 
first  part  of  the  arch,  the  latter  to  aneurysms  of  the  trans- 
verse and  descending  portions  of  the  arch. 

Physical  Signs  of  Aneurysm  in  general. 

The  most  important  and  conclusive  physical  sign  is 
pulsation  at  some  part  of  the  chest  wall  where  it  is  not 
normally  present.  We  must  of  course  make  sure  that  it  is 
not  due  to  the  heart  or  great  vessels  being  simply  un- 
covered or  displaced,  as  for  example  by  the  mediastinum 
being  dragged  to  the  right  in  consequence  of  retraction  of 
the  right  lung,  or  by  deformity  of  the  chest  wall  bringing 
the  heart  or  aorta  into  contact  with  the  chest  wall  in  some 
unusual  situation.  The  pulsation  may  or  may  not  be 
visible  ;  when  obscure  it  may  sometimes  be  made  more 
perceptible  by  pressing  firmly  on  the  part  and  watching 
the  hand  which  is  making  the  pressure ;  sometimes  it  can 
be  seen  by  standing  behind  the  patient  and  looking  over 
his  shoulders ;  it  may  be  recognizable  only  during  expira- 
tion ;  in  doubtful  cases  the  pulsation  may  sometimes  be 
rendered  evident  by  placing  the  small  end  of  a  wooden 
stethoscope  on  the  spot,  one  half  resting  on  a  rib,  the  other 
pressed  into  the  interspace,  when  the  stethoscope  will  be 
tilted. 

Pulsation  when  visible  may  be  a  localized  protrusion 
or  a  general  heave.  Generally  speaking  it  is  best  felt  by 
placing  the  palm  of  the  hand  flat  on  the  pulsating  area,  but 
it  may  be  necessary  to  press  the  fingers  well  into  the 
intercostal  spaces.  In  estimating  the  significance  of  pulsa- 
tion, whether  in  a  tumour  within  the  cavity  of  the  thorax, 


ANEURYSM  OF  THE  ARCH  OF  THE  AORTA.  435 

or  in  a  tumour  which  has  made  its  way  through  the  chest 
walls,  there  must  be  taken  into  account,  not  only  the 
degree  of  its  force  or  violence,  and  the  extent  of  the  area 
over  which  it  is  felt,  but  also  its  character,  that  is,  whether 
it  is  distinctly  expansile  in  some  or  all  directions,  or  is 
simply  firm  and  thrusting  without  marked  expansion.  In 
the  former  case  the  pulsating  tumour  will  feel  soft,  and 
there  will  be  no  laminated  fibrin  lining  supporting  its 
wall ;  in  the  latter  case  this  will  probably  be  present. 
These  conditions  have  an  important  bearing  on  the  probable 
progress  of  the  aneurysm,  and  consequently  on  the  question 
of  prognosis. 

A  characteristic  vibratory  thrill  may  be  present,  and  is 
best  felt  by  the  palm  of  the  hand  pressed  lightly  on  the 
tumour.  Another  point  to  be  ascertained  in  the  process  of 
palpation  is  the  presence  or  absence  of  a  diastolic  shock. 
This  is  a  sharp  vibration  or  shock,  felt  at  the  end  of  the 
true  pulsation,  synchronous  with  and  due  to  the  same  cause 
as  the  second  sound  of  the  heart,  viz.  the  recoil  of  the 
elastic  walls  of  the  aorta  from  the  distension  caused  by  the 
systolic  injection  of  blood.  This  diastolic  shock  is  the  most 
absolutely  pathognomonic  of  the  signs  of  aneurysm  ;  pulsa- 
tion may  be  communicated  to  a  tumour,  or  a  malignant 
growth  may  itself  be  pulsatile,  but  there  is  no  diastolic 
shock  under  such  conditions. 

The  fingers  may  have  to  be  pressed  into  intercostal 
spaces  to  recognize  pulsation  when  an  aneurysm  of  the 
ascending  aorta  is  just  projecting  from  under  the  right  edge 
of  the  sternum ;  usually  it  is  best  felt  at  the  end  of  expira- 
tion, when  the  border  of  the  lung  is  withdrawn  from  over 
the  vessel.  It  must  be  borne  in  mind  that  pulsation  can 
often  be  made  out  in  two  or  three  spaces  close  to  the  right 
of  the  sternum,  when  the  aorta  is  dilated  from  protracted 
high  tension,  or  from  incompetence  of  the  aortic  valves  :  it 
is  when  it  is  felt  in   one  space   only,   and   for   a  certain 


436  HEART  DISEASE. 

distance  beyond  the  edge  of  the  .sternum,  that  it  may  be 
accepted  as  significant  of  aneurysm.  More  rarely  can 
pulsation  to  the  left  of  the  manubrium  be  detected  in  this 
way  in  cases  of  aneurysm  of  the  transverse  portion  of  the 
arch. 

The  tracheal  tug  should  be  sought  for  while  carrying  out 
the  examination  by  palpation.  To  detect  this,  the  trachea 
is  put  gently  on  the  stretch,  by  the  fingers,  which  are 
placed  just  beneath  the  cricoid  cartilage  :  if  present  a 
distinct  short  tug  on  the  trachea  is  felt  with  each  cardiac 
systole,  superimposed  on  the  slower  up  and  down  movements 
in  respiration.  It  is  a  very  important  sign,  but  not 
absolutely  conclusive,  and  in  particular  it  does  not  help  to 
distinguish  between  a  sacculated  projection  from  the  aorta, 
and  a  general  dilatation  of  the  arch.  A  slight  shock  or 
communicated  pulsation  may  sometimes  be  felt  even  in 
cases  where  there  is  no  disease  of  heart  or  aorta. 

Percussion. — When  pulsation  is  distinct  the  evidence  to 
be  obtained  by  percussion  is  of  secondary  importance. 
Dulness  around  the  pulsating  area  will  merely  serve  to 
indicate  the  extent  of  the  aneurysm.  When  pulsation  is 
obscure,  or  absent,  deep  dulness  on  percussion  over  a  certain 
area  may  corroborate  and  reinforce  other  indications  of 
aneurysm,  and  be  of  great  diagnostic  value  ;  such  may  be 
especially  the  case  when  the  aneurysm  is  in  the  transverse 
or  descending  part  of  the  arch,  and  is  comparatively  small  : 
very  slight  physical  signs  may  be  then  of  great  importance 
in  the  interpretation  of  the  symptoms  present ;  the  area  of 
dulness  in  such  a  case  would  probably  be  situated  to  the 
left  of  the  manubrium  and  over  the  left  half  of  the  manu- 
brium itself. 

Auscultation. — Of  the  auscultatory  indications,  by  far 
the  most  important  is  a  low-pitched,  musical  second  sound, 
which,  when  well  marked,  is  loud  and  ringing.  It  is  coinci- 
dent with  the  diastolic  shock,  and  when  a  rigid  stethoscope 


ANEURYSM  OF  THE  ARCH  OF  THE  AORTA.  437 

is  employed  in  auscultation  the  shock  and  sound  will  be 
felt  and  heard  together.  The  significance  of  this  ringing, 
low-pitched  second  sound  is  greater,  the  more  remote  its 
point  of  maximum  intensity  from  the  aortic  valves — when, 
for  example,  it  is  heard  far  out  in  the  right  chest,  and 
especially  when  it  appears  to  the  left  of  the  manubrium  : 
a  reinforcement  and  change  in  character  of  the  second 
sound  in  the  course  of  the  aorta  can  scarcely  be  due  to  any 
other  cause  than  a  dilatation  or  aneurysm. 

This  aneurysmal  second  sound  is  not  simply  an  accentua- 
tion or  intensification  of  the  normal  aortic  second  sound  ; 
the  pitch  is  lower  from  the  fact  that  the  wall  of  the  sac 
constitutes  a  larger  area  of  resonating  membrane  than  the 
tube  of  the  aorta.  The  second  sound  is  not  produced  by  a 
click  of  the  semi-lunar  valves  or  by  their  sudden  tension, 
but  by  the  sudden  tension  of  the  walls  of  the  aorta  and 
valves  together,  as  a  vibrating  membrane.  When  the 
aortic  valves  are  incompetent,  the  aneurysmal  second  sound 
is  impaired,  but  rarely  extinguished. 

The  difference  in  the  character  and  mode  of  production 
of  the  aortic  and  the  aneurysmal  second  sound  may  be 
illustrated  by  suddenly  putting  on  the  stretch  a  small 
length  of  linen  (say  three  inches  of  the  border  of  a  pocket- 
handkerchief)  and  comparing  the  sound  thus  produced  with 
that  which  is  generated  when  a  portion  double  the  length 
is  similarly  put  on  the  stretch.  In  the  latter  instance  the 
sound  is  lower  pitched,  of  greater  volume,  less  sharp  in 
character  than  in  the  former,  and  corresponds  to  the 
aneurysmal  second  sound. 

A  murmur  may  or  may  not  be  heard  in  aneurysm. 
When  present  over  a  pulsating  area,  it  adds  nothing  to  the 
value  of  other  physical  signs,  since  a  tumour  pressing  upon 
the  aorta,  or  one  of  its  branches,  may  give  rise  to  a  murmur, 
and  its  absence  does  not  detract  from  their  significance. 
Sometimes  when  no  murmur  is  heard  over   the  aneurysm 


438  HEART  DISEASE. 

itself,  one  may  be  heard  on  the  distal  side  of  the  sac, 
caused  by  pressure  on  the  aorta  beyond  it  or  on  some  of 
its  branches.  A  murmur  may  be  a  sign  of  great  value 
when,  being  absent  over  the  aortic  area,  it  is  developed  in 
the  course  of  the  arch  and  becomes  audible  over,  or  to  the 
left  of,  the  manubrium. 

The  auscultatory  signs  resulting  from  pressure  on  the 
root  of  one  or  other  lung,  will  not  be  discussed  here,  but 
mention  must  be  made  of  tracheal  breath  sounds  conducted 
to  the  manubrium  by  means  of  an  aneurysm  in  contact  with 
the  trachea ;  these  may  be  heard  over  this  bone  loudly 
and  distinctly  before  serious  pressure  is  produced  by  the 
aneurysm  on  the  trachea. 

The  Pulse. — An  aneurysm  may  give  rise  to  characteristic 
modification  of,  or  difference  between  the  two  radial  pulses. 

The  sac  of  an  aneurysm  is  readily  distended,  and  has 
little  contractile  power  or  elastic  recoil,  and  its  interposition 
in  the  course  of  the  aorta  will  impair  and  delay  the  pressure 
or  pulse-wave  which  is  transmitted  with  great  rapidity  at 
each  systole  of  the  heart  throughout  the  arterial  system. 

The  combined  effect  on  the  pulse-wave  will  be,  firstly  to 
delay  it,  secondly  to  diminish  its  height,  thirdly  to  cause 
its  duration  to  be  longer,  and  its  subsidence  more  gradual 
and  slower  than  normal. 

As  a  further  consequence,  the  artery  will  also  be  con- 
stantly full  between  the  beats,  as  the  sac  acts  like  a  black- 
smith's bellows — being,  in  fact,  a  reservoir  of  blood. 

These  points  are  well  illustrated  by  the  sphygmographic 
tracings  appended  (Figs.  29  and  30). 

It  is  obvious  that  if  the  aneurysm  is  situated  in  the 
ascending  aorta,  it  will  affect  both  pulses  alike,  and  as  there 
will  then  be  no  standard  of  comparison,  such  modification  of 
the  pulse,  if  it  exist,  will  be  of  no  great  help  in  diagnosis. 
Moreover,  the  modification  of  the  pulse  is  not,  as  a  rule,  so 
striking  as  to  attract  attention. 


ANEURYSM  OF  THE  ARCH  OF  THE  AORTA.  439 

Difference  between  the  two  radial  pulses  is,  however, 
frequently  one  of  the  most  important  physical  signs  in 
diagnosis  of  aneurysm,  and  may  be  present  in  the  earlier 
stages,  before  pulsation  is  visible. 

Difference  between  the  pulses  may  arise  :  (1)  From 
partial  blocking  of  the  mouth  of  one  of  the  main  branches 
of  the  aorta  given  off  from  an  aneurysmal  sac  by  projection 
into  it  of  a  portion  of  fibrin  from  the  organized  deposit  on 
the  walls  of  the  sac.  (2)  From  pressure  on  the  innominate,  or 
one  of  the  sub-clavian  arteries  by  an  aneurysm  ;  one  of  these 


Walter  Bioadbent,/eci't. 

FIG.  29.— LEFT   KADIAL    PULSE   IN    ANEURYSM   OF    ASCENDING    AORTA    INVOLVING   ORIFICE 
OF   INNOMINATE   ARTERY. 


FIG.    oO.— RIGHT   RADIAL   PULSE   IN   SAME   CASE. 

vessels  may  even  be  involved  in  the  sac  and  run  in  its  walls, 
so  that  its  lumen  becomes  partially  or  totally  obliterated. 
For  instance,  the  right  radial  artery  may  be  smaller  than 
the  left,  and  the  pulsation  in  it  weakened  or  altered  in 
character,  or  entirely  absent,  from  pressure  of  an  aneurysm 
on  the  innominate  artery,  or  from  obstruction  of  its  orifice. 
More  frequently  it  is  the  left  pulse  which  is  affected,  either 
by  the  interposition  of  an  aneurysm  between  the  origin  of 
the  innominate  and  the  left  sub-clavian  artery,  or  by  the 


44° 


HEART  DISEASE. 


latter  being  given  off  from  the  aneurysmal  sac  itself.  In 
such  a  case  the  left  radial  pulse  will  present  all  the 
characters  of  the  aneurysmal  pulse  above  described,  while 
the  right  radial  pulse  will  be  unaffected,  and  the  difference 
between  the  two  pulses  may  be  very  marked,  as  will  be  seen 
in  the  tracings  (Figs.  31  and  32).  It  is  important,  however, 
to  remember  that  difference  between  the  pulses  at  the  wrist 
may  arise  from  other  causes  than  aneurysm.  The  calibre  of 
the  radial  arteries  on  the  two  sides  may  be  different ;  some- 
times the  radial  artery  is  smaller  in  one  arm  than  the  other, 


FIG.    31. — LEFT   RADIAL   IN   ANEURYSM    OF   AORTA    INVOLVING    ORIFICE 
OF   LEFT-CLAVIAN. 


FIG    32— EIGHT   RADIAL    IN    SAME   CASE,   UNAFFECTED. 

and  the  ulnar  artery  larger  by  way  of  compensation.  Or 
the  radial  artery  may  turn  round  prematurely  to  the  dorsal 
aspect  of  the  limb,  being  represented  at  the  wrist  only  by 
a  small  branch,  the  superficialis  volse.  A  real  difference 
between  the  two  pulses  may  be  caused  by  pressure  of  a 
tumour  on  any  part  of  the  arterial  channel  of  which  the 
radial  is  a  branch — sub-clavian,  axillary,  brachial.  Again, 
the  orifice  of  the  innominate  or  of  the  left  sub-clavian  may 
be  partially  occluded  by  a  calcareous  deposit,  the  result  of 
atheromatous  changes. 

In  a  case  that  was  under  my  care  at  St.  Mary's  Hospital 
in  1893,  the  difference  in  the  character  of  the  two  radial 
pulses  was  so  marked  and  so  typical  of  aneurysm  that  there 


ANEURYSM  OF  THE  ARCH   OF  THE  AORTA.  44 1 

seemed  to  be  no  escape  from  a  diagnosis  of  aneurysm  of 
the  transverse  part  of  the  arch  involving  the  orifice  of  the 
left  sub-clavian  {vide  tracings  Figs.  33  and  34).  The  patient 
was  fifty-eight  years  of  age,  and  was  admitted  for  shortness 
of  breath  and  severe  pain  in  the  precordial  region.  The 
heart  was  hypertrophied,  and  there  was  a  double  aortic 
murmur.  There  was  no  pulsation  visible  over  the  aortic  or 
pulmonic  area,  and  no  dulness  on  percussion.  There  was, 
in  fact,  no  other  physical  sign  of  aneurysm,  except   the 


FIG.  00.— LEFT   RADIAL   PLLSE,   IN   CASE    WHERE   ORIFICE   OF   LEFT   SLB-CLAVIAN 
WAS   OBSTRUCTED   BY   ATHEROMA. 


FIG.  34. — RIGHT    RADIAL   PDLSE. 

marked  difference  in  the  pulses,  though  the  severe  pain 
in  the  chest  and  paroxysms  of  dyspnoea  were  symptoms  con- 
sistent with,  and  in  favour  of  aneurysm.  At  the  post-mortem 
no  aneurysm  was  found,  but  the  orifice  of  the  left  sub-clavian 
artery  was  about  one-half  occluded  by  a  thick  calcareous 
plate  projecting  across  it.  The  aorta  was  also  dilated  and 
atheromatous,  and  the  aortic  valves  were  incompetent. 

Delay  of  Pulse. —  One  of  the  most  characteristic  differ- 
ences between  the  two  radial  pulses  which  may  be  present 
in  aneurysm  is  the  apparent  delay  in  one,  when  they  are 
both  felt  at  the  same  time.  If  one  is  affected  by  the 
interposition  of  the  aneurysmal  sac,  the  rise  in  pressure  is 
more  gradual,  and  reaches  its  maximum  later ;  and  as  this 
is  what  is  felt  as  the  pulse,  it  will  be  delayed  as  compared 
with  that  of  the  other  side. 


442  HEART  DISEASE. 

The  Carotid  Arteries. — It  must  be  borne  in  mind  also 
that  an  aneurysm  may  affect  pulsation  in  the  carotids  in 
the  same  way  as  in  the  radials.  For,  the  orifice  of  the 
left  carotid  may  be  involved  in  the  sac,  or  may  be  parti- 
ally occluded  by  a  plug  of  fibrin,  and  it  is  obvious  that 
whatever  affects  the  innominate  artery  will  similarly  affect 
the  right  sub-clavian  and  right  carotid.  The  blocking  of 
one  carotid,  partial  or  complete,  or  a  difference  between  the 
pulsation  in  the  carotids  on  either  side,  corresponding  to 
that  already  noted  in  the  radials,  will  be  important  con- 
firmatory evidence  of  aneurysm. 

The  Heart. — It  has  been  asserted  by  some  authorities 
that  aneurysm  gives  rise  to  hypertrophy  of  the  heart.  That 
this  is  not  the  case  has  been  conclusively  shown  by  Dr. 
James  Calvert,*  in  a  paper  based  on  an  analysis  of  124  cases 
of  aneurysm  collected  by  Dr.  Oswald  Browne.  In  68  of  these 
cases  aneurysm  existed  without  giving  rise  to  any  hypertrophy 
of  the  heart.  It  is,  however,  true  that  cardiac  hypertrophy 
is  not  infrequently  found  in  association  with  aneurysm,  but 
it  may  almost  invariably  be  explained  by  causes  other 
than  aneurysm,  such  as  arterio-sclerosis  or  prolonged  high 
arterial  tension  due  to  kidney  disease  or  other  causes. 

The  heart  may  be  displaced  by  aneurysm  of  the  ascending 
aorta,  or  of  the  transverse  part  of  the  arch,  so  that  the  apex 
beat  may  be  found  below  and  outside  its  normal  position, 
but  this  should  not  be  mistaken  for  hypertrophy.  More 
frequently  the  apex  beat  is  displaced  upwards  :  its  position, 
and  the  extent  to  which  the  heart  is  displaced,  will  vary 
according  to  the  size,  shape,  and  situation  of  the  aneurysm. 

The  physical  signs  that  have  been  discussed  thus  far  are 
mainly  those  directly  dependent  on  the  aneurysm  itself, 
produced  in  and  by  it,  and  not  on  indirect  or  pressure  effects 
of  the  aneurysm  on  adjacent  structures,  which  will  now  be 
considered. 

*  Trans.  Med.  Chir.  Soc,  1891). 


aneurysm  of  the  arch  of  the  aorta.         443 

Pressure  Effects  of  Aneurysm  on  Adjacent 
Structures. 

1.  Ths  Great  Veins. — An  aneurysm  may  compress  and 
cause  obstruction  to  the  flow  of  blood  through  one  of  the 
large  venous  trunks,  the  vena  cava  superior,  or  the  right 
or  left  innominate  veins. 

A  sudden  and  complete  block  of  the  vena  cava  superior 
from  thrombosis,  or  from  compression  by  sudden  extension 
of  the  aneurysm,  may  give  rise  to  oedema  of  the  head 
and  neck  and  upper  extremities,  with  a  cyanotic  appear- 
ance, the  face  being  enormously  swollen  and  disfigured, 
while  severe  dyspnoea  is  produced  by  oedema  of  the  fauces 
and  larynx.  This,  however,  is  an  extremely  rare  event, 
only  one  example  having  come  under  my  observation. 
Usually,  the  pressure  takes  effect  gradually,  and  collateral 
venous  channels  are  developed  which  carry  the  blood  from 
the  tributaries  of  the  superior  vena  cava  to  the  inferior,  and 
obviate  the  effect  described.  Some  of  these  are  external, 
in  the  form  of  large  tortuous  veins  crossing  the  clavicles, 
descending  the  surface  of  the  chest,  sometimes  continued 
down  the  abdomen.  A  remarkable  instance  of  this  is 
shown  in  the  photograph  (Fig.  35)  taken  from  a  case  of 
aneurysm  of  the  first  part  of  the  arch,  which  was  under 
observation  for  upwards  of  six  years.  The  mass  of  dilated 
veins,  some  of  which  were  of  the  size  of  the  finger,  on  the 
surface  of  and  below  the  tumour,  was  a  striking  feature. 
Below  the  mamma  many  of  these  veins  disappeared,  pre- 
sumably anastomosing  with  the  intercostal  veins,  but  three 
large  tortuous  veins  continued  downward  to  anastomose 
apparently  with  the  right  epigastric  veins.  The  direction 
of  the  current  of  blood,  which  should  always  be  carefully 
ascertained,  was  found  to  be  downwards.  Other  channels 
of  communication,  in  which  the  azygos  veins  take  part,  are 
deep  seated  and  not  open  to  observation.     The  proportion 


444  HEART  DISEASE. 

of  superficial  and  deep  collateral  venous  circulation  varies 
greatly  in  different  cases. 

The  jugulars  are  distended,  and  an  important  point 
is  that  they  are  not  emptied  even  partially  by  a  deep 
inspiration,  as  is  the  case,  more  or  less,  when  the  veins 
of  the  neck  are  full  from  back  pressure  in  the  systemic 
venous  system  in  mitral  disease,  or  in  emphysema  and 
bronchitis. 


FIG.  35. — TOBTOOOS   DILATED    VEINS   ON   SURFACE   OF   LARGE   ANEURYSM   OF 
ASCENDING  AORTA. 

Again,  there  is  no  true  jugular  pulsation  such  as  is 
present  in  venous  reflux  from  the  tricuspid  incompetence 
which  supervenes  as  a  result  of  dilatation  of  the  right 
ventricle  in  mitral  disease  or  emphysema.  There  may, 
however,  be  apparent  pulsation  in  the  veins  caused  by  the 
subjacent  carotid. 

There  may  be  pressure  on  the  azygos  vein  which  passes 
up   behind   the  root  of  the  right   lung   to  open  into  the 


ANEURYSM  OF  THE  ARCH  OF  THE  AORTA.  445 

superior  vena  cava  just  before  it  enters  the  pericardium. 
This,  does  not  appear  to  give  rise  to  any  characteristic 
physical  signs  or  symptoms,  probably  because  of  the  free 
anastomosis  with  the  lumbar  veins,  which  enables  the  blood 
to  return  without  difficulty  via  the  iliac  veins  and  inferior 
vena  cava. 

Even  more  interesting  than  obstruction  of  the  vena  cava 
is  obstruction  of  one  or  other  of  the  innominate  veins.  The 
discovery  of  a  one-sided  distension  of  the  external  and 
anterior  jugulars,  not  disappearing  in  deep  inspiration, 
especially  if  associated  with  dilatation  of  the  veins  of  the 
upper  extremity,  is  not  unfrequently  the  first  step  towards 
the  diagnosis  of  an  aneurysm  which  might  otherwise  have 
eluded  detection  for  some  time.  In  such  a  case  the  col- 
lateral enlargement  of  veins  is  also  one-sided. 

2.  Pressure  on  the  Root  of  the  Lung. — Pressure  on  the 
right  or  left  bronchus  will  cause  diminished  entry  of  air  to 
the  corresponding  lung,  with  characteristic  alteration  of  the 
breath  sounds.  When  the  bronchus  is  obstructed  without 
pressure  on  the  pulmonary  veins,  the  resonance  will  not 
be  impaired,  or  will  be  only  slightly  modified.  Eesonance 
on  percussion  in  association  with  silence  on  auscultation 
(pneumothorax,  of  course,  being  excluded)  are  highly 
characteristic  of  obstruction  of  a  bronchus.  The  collap>se 
of  lung  which  eventually  ensues  will  give  rise  to  some 
falling  in  of  the  intercostal  spaces,  and  impairment  of 
resonance. 

Pressure  on  the  pulmonary  veins  may  occur,  giving 
rise  to  congestion  of  the  lung  tissue.  As  a  rule,  however, 
they  escape  compression  in  spite  of  their  unresisting 
structure,  probably  because  they  are  protected  by  the 
bronchi  which  usually  suffer  first.  One  case,  nevertheless 
has  come  under  my  notice  in  which  the  lung  was  found  at 
the  autopsy  to  be  in  a  semi-gangrenous  condition  from  this 
cause.     The  aneurysm  was  a  large  one,  about  the  size  of 


446  HEART  DISEASE. 

two  fists,  affecting  the  ascending  aorta  and  extending  back- 
wards, and  compressing  the  root  of  the  right  lung  as  well 
as  presenting  on  the  chest  wall  as  a  pulsating  tumour. 

3.  Pressure  on  the  cilio-spinal  branches  of  the  sympa- 
thetic may  cause  dilatation  or  contraction  of  the  pupil  on 
the  corresponding  side  according  as  the  dilator  fibres  are 
irritated  or  destroyed  by  compression. 

4.  Pressure  on  the  left  recurrent  laryngeal  nerve  will 
cause  paralysis  of  the  left  vocal  cord. 

The  right  recurrent  laryngeal  nerve  is  seldom  affected 
by  aneurysm  of  the  aorta,  since  it  winds  round  the  right 
sub-clavian  artery  ;  occasionally  it  may  be  subjected  to 
pressure  by  the  sac  of  an  aneurysm  of  the  transverse  part 
of  the  arch  involving  the  orifice  of  the  innominate,  or  by 
extension  upwards  of  an  aneurysm  of  the  ascending  part 
of  the  arch. 

5.  Pressure  on  the  trachea,  oesophagus,  and  thoracic 
duct  may  be  caused  by  an  aneurysm  of  the  transverse  or 
descending  part  of  the  arch. 

There  remains  for  discussion  one  symptom,  namely  pain, 
which  is  usually,  at  some  period  in  the  history  of  an 
aneurysm,  a  conspicuous  feature. 

Pain  is  very  rarely  absent,  though  it  differs  greatly  in 
character  and  intensity  in  different  cases.  A  feature 
common  to  aneurysmal  pain  of  all  kinds  and  in  any 
situation,  is  the  aggravation  of  it  by  exertion. 

Pain  may  be  the  sole  symptom,  and  may  be  of  itself, 
without  corroboration  by  physical  signs,  sufficient  for  a 
diagnosis  of  aneurysm. 

Aneurysm  at  the  very  root  of  the  aorta  within  the  cavity 
of  the  pericardial  sac,  or  aneurysm  of  the  sinuses  of  Valsalva, 
may  give  rise  to  pain  of  anginoid  character.  It  may 
indeed  cause  true  angina  by  extension  of  disease  from  the 
sinuses  of  Valsalva  along  the  coronary  arteries,  or  by 
obstructing  the  openings  of  these  vessels  and  consequently 


ANEURYSM  OF  THE  ARCH  OF  THE  AORTA.  447 

giving  rise  to  degeneration  of  the  walls  of  the  heart.  It 
is  not  always  possible  to  distinguish  between  anginoid 
pain  due  to  aneurysm  in  this  situation  and  true  angina; 
the  sense  of  impending  death  is  not  as  a  rule  so  marked 
a  feature  of  the  attacks,  and  the  pain  often  radiates  down 
both  arms  instead  of  along  the  left  only ;  occasionally 
it  shoots  down  the  right  arm  only.  In  angina,  there  may 
be  no  physical  signs  of  disease  in  the  great  vessels ;  in 
aneurysm  there  will  be  the  ringing  second  sound,  and 
frequently  a  diastolic  murmur,  but  rarely,  dulness  nn  per- 
cussion or  recognizable  pulsation. 

In  aneurysm  of  the  ascending  aorta,  there  is  usually 
deep-seated  pain  of  a  vague  kind  which  may  be  very  severe 
while  the  aneurysm  is  extending,  and  may  become  quiescent 
when  it  has  ceased  to  enlarge.  It  is  usually  aggravated 
by  certain  positions,  relieved  by  others,  so  as  to  constrain 
the  patient  to  a  particular  decubitus,  different  in  different 
cases  without  obvious  reasons.  Pain  in  the  right  shoulder 
or  scapular  region  may  indicate  backward  extension  of 
an  aneurysm  of  the  ascending  aorta  which  is  not  revealed 
by  physical  signs. 

Pain  again  attends  the  process  of  penetration  of  the 
chest  wall,  though  it  need  not  be  severe.  When  the 
barrier  of  the  ribs  is  overcome  and  the  aneurysm  projects  on 
the  surface  of  the  chest,  there  is  often  relief,  not  only  from 
the  pain  attending  the  pressure  forward  on  the  thoracic 
parietes,  but  from  deep-seated  pain. 

A  remarkable  pain  sometimes  attends  aneurysm  in  this 
situation,  located  in  the  tip  of  the  right  shoulder,  and  at 
the  occipital  insertion  of  the  trapezius.  When  very  severe, 
I  have  found  the  trapezius  muscle  in  a  state  of  spasm,  and 
the  head  slightly  rotated  ;  but  pain  may  be  present  when 
the  muscular  spasm  is  slight.  Apparently  the  cause  is 
reflex  irritation  of  the  spinal  accessory  nerve. 

There   is  nothing  specially  remarkable  about  the  pain 


448  HEART  DISEASE. 

attending  aneurysm  of  the  transverse  part  of  the  arch, 
though  it  is  often  severe.  It  is  when  the  descending  part 
of  the  arch,  or  the  thoracic  aorta  is  the  seat  of  aneurysm, 
that  pain  may  be  the  sole  symptom.  The  vessel  is  firmly 
held  down  to  the  vertebral  column  by  the  intercostal 
arteries ;  erosion  of  the  bodies  of  the  vertebras  takes  place, 
and  the  intercostal  nerves  may  be  reached.  Lancinating 
pain  is  then  experienced  of  an  extremely  severe  and  per- 
sistent character  before  the  aneurysm  has  reached  a  size 
which  permits  of  its  recognition  by  physical  signs. 

Thus  far  we  have  enumerated  the  general  physical  signs 
and  symptoms  to  which  aneurysm  of  the  arch  of  the  aorta 
may  give  rise.  We  shall  now  proceed  to  group  these 
together  around  the  various  clinical  types  of  aneurysm  of 
which  they  are  severally  characteristic. 

Classification  of  Aneurysms  of  the  Aech  of 
the  Aoeta. 

For  clinical  purposes  we  may  divide  aneurysms  of  the 
aorta  into  four  groups,  according  to  their  anatomical 
situation — 

(1)  Aneurysm  of  the  intra-pericardial  portion  of  the 
aorta ; 

(2)  Of  the  ascending  aorta  as  far  as  the  origin  of  the 
innominate ; 

(3)  Of  the  transverse  part  of  the  arch  ; 

(4)  Of  the  descending  part  of  the  arch. 

(1)  Aneurysm  of  the  Intra-pericardial  Portion 
of  the  Aorta. 

The  favourite  site  of  an  intra-pericardial  aneurysm  is 
one  of  the  sinuses  of  Valsalva.  As  there  are  no  adjacent 
structures  to  support  the  sac  and  contribute  to  its  wall, 
it  usually  ruptures  into  the  pericardium  before  it  attains 


ANEURYSM  OF  1NTRA-FERICARD1AL  PART  OF  AORTA.      449 

any  considerable  size.  Should  the  aneurysm,  however, 
extend  towards  the  pulmonary  artery  or  superior  vena 
cava,  its  sac  may  become  adherent  to  their  wall,  so  that 
rupture  is  deferred  for  a  time,  eventually  taking  place, 
as  a  rule,  into  one  of  these  vessels. 

Physical  Signs  and  Symptoms. — Angina  pectoris  may 
be  present  if  the  aneurysm  involves  the  orifice  of  one  of 
the  coronary  arteries,  but  frequently  no  physical  signs  or 
symptoms  are  present,  and  sudden  death  occurs  from 
rupture  of  the  aneurysm  into  the  pericardium  before  any 
suspicion  as  to  its  presence  has  been  aroused. 

It  may  so  happen  that  the  sac  of  the  aneurysm 
compresses  the  superior  vena  cava  and  obstructs  the 
return  of  blood  to  the  heart  through  this  vessel,  thus  giving 
rise  to  characteristic  symptoms. 

An  interesting  instance  of  the  latter  condition  occurred  in  a  case 
under  my  care  at  St.  Mary's  Hospital  in  1893.  The  patient,  a  man 
aged  30,  was  admitted  suffering  from  shortness  of  breath  and  pain  of 
an  anginoid  character.  On  examination,  the  heart  was  found  to  be 
hypertrophied,  and  there  was  evidence  of  aortic  and  mitral  incompe- 
tence. The  veins  of  the  neck  were  distended  and  full,  and  it  was 
noted  that  they  did  not  empty  on  deep  inspiration.  This  seemed  to 
indicate  that  some  tumour  pressing  on  the  superior  vena  cava,  possibly 
aneurysm,  was  the  cause  of  the  obstruction  to  the  return  of  blood  to 
the  heart.  The  liver  was  not  enlarged,  and  there  was  no  oedema  of 
the  extremities,  so  that  it  was  clear  there  was  no  obstruction  to  the 
return  of  blood  by  the  infei*ior  vena  cava.  There  was,  however,  no 
other  definite  evidence  of  aneurysm  at  the  time  of  his  admission,  but 
on  February  19th,  a  month  later,  he  had  an  attack  of  severe  pain  in  the 
region  of  the  heart,  and  became  very  pale  and  almost  pulseless ;  he 
rallied  from  this  state  of  collapse,  and  in  the  evening  vomited  a  little 
blood.  Signs  of  pericardial  effusion  were  present,  and  it  was  thought 
that  a  small  rupture  of  the  aneurysm  into  the  pericardium  had  taken 
place. 

He  died  four  days  later,  becoming  suddenly  very  pale  and  falling 
back  dead  in  bed.  At  the  autopsy  the  pericardium  was  found  to  be 
full  of  blood  and  recent  clot,  and  there  was  also  pale  firm  clot  of  older 
date  due  to  the  haemorrhage  four  days  before  death. 

There  was  a  small  aneurysm  on  the  outer  aspect  of  the  aorta  about 
one  and  a  quarter  inch  above  the  valves,  bulging  into  and  partially 
embedded  in  the  superior  vena  cava  just  below   the   point  where  it 

2  G 


450  HEART  DISEASE. 

entered  the  pericardium.     This  had  ruptured,  and  caused  the  sudden 
death. 


Eupture  op  an  Aneurysm  into  the  Pulmonary 
Artery. 

A  considerable  number  of  cases  of  this  incident  have 
been  recorded.  In  1840  *  Thurnam  recorded  five  cases  ; 
in  1897  f  Lamplough  published  a  case  which  came  under 
his  observation,  and  gave  a  brief  summary  of  fifteen  cases 
which  he  had  been  able  to  collect,  six  of  which  had  been 
published  in  the  Transactions  of  the  Pathological  Society. 
In  1899  Sir  William  G-airdner  published  a  case  in  the 
Glasgow  Hospital  Reports,  and  in  1900  %  Michell  Clarke 
recorded  a  case.  We  have,  therefore,  although  the  con- 
dition is  rare,  a  sufficient  number  of  cases  recorded  for 
diagnostic  data. 

Physical  Signs  and  Symptoms. — The  immediate  symptoms 
of  rupture  are,  sudden  pain  in  the  chest  with  severe  dyspnoea, 
followed  by  cough,  sometimes  with  expectoration  of  blood- 
stained mucus.  The  attack  does  not,  as  a  rule,  prove 
rapidly  fatal,  but  the  patient  may  survive  some  weeks  or 
several  months,  when  definite  physical  signs  and  symptoms 
will  usually  develop.  The  earliest  fatal  termination  in 
Lamplough's  cases  was  in  two  weeks.  The  longest  survival 
one  year. 

The  most  characteristic  physical  sign  is  a  continuous 
roaring  murmur,  audible  over  the  second  and  third  left 
intercostal  spaces.  The  murmur  is  loud  and  vibratory,  its 
maximum  intensity  being  systolic  in  time. 

A  vibratory  thrill  may  sometimes  be  felt  on  palpa- 
tion over  the  pulmonic  area,  and  was  present  in  6  per 
cent,   of  Lamplough's    cases.      Pulsation    is    not    present. 

*  Trans.  Meil.  Chi.  Soc,  vol.  xxiii.  p.  323. 
t  B.  M.  J.,  1897,  vol.  ii.  p.  392. 
%  B.  M.  J.,  1900,  vol.  ii.  p.  1701. 


ANEURYSM  OF  INTRA- PERICARDIAL  PART  OF  AORTA.      451 

Subsequently,  symptoms  of  dilatation  of  the  right  ventricle 
develop,  and  as  this  gives  way,  enlargement  of  the  liver, 
tricuspid  incompetence,  and  dropsy  supervene,  with  en- 
gorgement of  the  lungs,  and  the  patient  dies  with  all  the 
symptoms  of  right  ventricle  failure. 

I11  a  case  recently  under  tlis  care  of  Dr.  Lees  at  St.  Mary's  Hospital, 
the  patient  was  a  man  aged  49,  who,  ten  months  before  admission, 
was  suddenly  seized  with  pain  in  the  chest  and  severe  dyspnoea.  Three 
months  after  this  attack,  ascites  and  oedema  of  the  legs  set  in.  He  was 
tapped  for  ascites  seven  times.  On  admission  to  St.  Mary's  Hospital, 
ten  months  after  the  onset  of  symptoms  pointing  to  rupture  of  the 
aneurysm  into  the  pulmonary  artery,  there  was  dyspnoea,  slight 
cyanosis,  dropsy,  and  ascites.  Over  the  second  and  third  intercostal 
spaces  to  the  left  of  the  sternum  there  was  a  well-marked  vibratory 
thrill,  but  110  actual  pulsation.  Over  this  area  was  a  ceaseless,  loud, 
roaring  murmur,  varying  in  intensity  and  most  marked  over  the  third 
left  space.  There  was  some  hypertrophy  of  the  left  ventricle  and 
great  dilatation  of  the  right.  He  died  five  weeks  after  admission. 
Post-mortem  there  was  found  to  be  a  perforation  in  the  aorta  about 
half  an  inch  in  diameter,  which  opened  into  the  pulmonary  artery, 
obliterating  one  of  the  cusps  of  the  pulmonic  valve. 

Rupture  of  an  Aneurysm  into  the  Superior 
Vena  Cava. 

An  interesting  series  of  twenty-five  cases,  which  they 
have  collected  from  various  sources,  is  recorded  by  Pepper 
and  Griffiths.*  Death  frequently  occurs  in  a  few  hours' 
time,  but  the  patient  may  survive  some  months.  The 
shortest  period  in  which  death  occurred  was  six  hours ;  the 
longest  survival,  seven  months.  One  case  is  said  to  have 
recovered. 

Physical  Signs  and  Symptoms. — The  immediate  symptoms 
are  sudden  onset  of  severe  dyspnoea,  cyanosis,  turgescence 
of  the  veins  of  the  neck,  rapidly  followed  by  tense  oedema 
of  the  neck  and  face.  There  is  usually  little  or  no  actual 
pain.  The  dyspnoea,  cyanosis,  and  oedema  of  the  neck 
and  face  persist ;  distended  veins  make  their  appearance 
*  American  Journal  of  Medical  Sciences,  1890,  vol.  100,  p.  329. 


452  HEART  DISEASE. 

on  the  front  of  the  chest  from  collateral  circulation 
established  between  the  internal  mammary  and  the  inter- 
costal and  superficial  epigastric  veins.  In  course  of  time 
(from  two  to  five  weeks)  a  murmur  develops,  audible  over 
the  aortic  area.  The  murmur  may  be  systolic  in  time,  or 
continuous,  or  a  double  murmur,  systolic  and  diastolic,  may 
be  present.  Pulsation  over  this  area  may  make  its  appear- 
ance at  a  considerably  later  date,  and  is  present  in  about 
50  per  cent,  of  cases.  A  thrill  is  felt  in  the  majority  of 
cases,  but  not  in  all. 

The  following  case,  which  was  under  the  care  of  Dr.  Cheadle,  at 
St.  Mary's  Hospital,  in  1903,  is  of  exceptional  interest  in  that  it  was 
under  observation  from  the  onset  of  symptoms  till  death,  some  four 
months  later,  and  a  correct  diagnosis  was  made  on  the  day  of  admission. 

Thomas  M.,  aged  59,  admitted  to  St.  Mary's  Hospital,  March  28th, 
1903. 

History.— Was  well  till  the  evening  before  admission,  when  he 
suddenly,  while  in  bed,  became  very  short  of  breath  and  cyanosed. 
This  was  rapidly  followed  by  swelling  of  the  neck  and  face.  There  was 
no  history  of  any  previous  symptoms  pointing  to  aneurysm  or  affection 
of  the  heart. 

On  admission  next  morning  he  was  very  cyanosed  and  short 
of  breath.  The  neck  was  swollen,  brawny,  and  tense,  somewhat 
resembling  the  condition  of  angina  Ludovici,  and  did  not  pit  on 
pressure.  The  face  was  also  swollen,  more  especially  the  right  side. 
The  veins  in  the  neck  were  full  and  distended.  There  was  no  pulsa- 
tion visible,  and  no  murmur  was  audible  over  the  pulmonic  area. 

In  the  course  of  a  week  distended  tortuous  veins  made  their  appear- 
ance on  the  front  of  the  chest,  and  later  all  over  the  back  above  the 
scapulae.     The  current  of  blood  was  downwards. 

After  three  weeks  a  soft,  blowing  systolic  murmur  became  audible 
over  the  aortic  area,  which  gradually  increased  in  intensity  and  became 
more  prolonged.  It  remained  soft  and  blowing  and  never  became 
continuous,  though  the  diastolic  interval  was  very  short. 

A  month  after  admission  the  oedema  of  the  face  and  neck  had,  to 
a  great  extent,  subsided,  but  the  cyanosis  persisted  :  the  veins  over  the 
chest  and  back  were  very  prominent,  forming  a  diffuse  network  over 
the  whole  of  the  upper  part  of  the  front  of  the  chest.  The  right 
internal  jugular  vein  was  thrombosed  and  filled  with  firm  clot.  The 
dyspnoea  was  less  severe,  and  he  was  so  much  better  that  he  insisted 
on  going  home. 

He  was  readmitted  three  weeks  later  with  severe  dyspnoea, 
cyanosis,  and  oedema  of  the  right  arm  and  right  side  of  the  chest. 


ANEURYSM  OF  INTRA-PERICARDIAL  PART  OF  AORTA.      453 

The  murmur  over  the  aortic  area  was  louder  and  more  prolonged. 
He  became  noisy  and  delirious  at  night,  and  his  mental  faculties  were 
much  impaired.  Slight  pulsation  became  evident  over  a  localized  area 
in  the  second  right  intercostal  space.  He  died  on  May  10th,  four  and 
a  half  months  after  the  onset  of  symptoms. 

At  the  autopsy  an  aneurysm  was  found  springing  from  the  ascend- 
ing aorta  about  one  inch  from  its  origin.  The  sac  of  the  aneurysm  was 
about  three  inches  in  diameter,  and  the  pericardium  was  stretched  over 
its  upper  aspect.  There  was  a  communication  between  the  aneurysm 
and  the  superior  vena  cava  about  half  an  inch  in  diameter.  The 
sac  of  the  aneurysm  was  firmly  united  to  the  vena  cava  by  adhesions, 
and  there  was  no  leakage  into  the  pericardial  cavity.  The  superior 
vena  cava  was  greatly  dilated,  being  nearly  an  inch  in  diameter,  and 
its  walls  were  greatly  thickened.  The  right  internal  jugular  vein 
was  thrombosed,  and  occupied  by  firm  adherent  white  clot.  The  left 
innominate  vein  was  stretched  over  the  front  of  the  sac  of  the  aneurysm, 
and  its  lumen  was  entirely  obliterated.  The  right  innominate  and  sub- 
clavian veins  and  the  left  sub-clavian  and  internal  jugular  veins  were 
patent  and  free  from  clot.  The  azygos  vein  was  greatly  enlarged. 
The  aorta  was  atheromatous. 


KUPTURE  OF  AN  ANEURYSM  INTO  THE  AURICLES. 

Cases  are  on  record  in  which  an  aneurysm  has  ruptured 
into  one  of  the  auricles.  In  one  case  of  rupture  into  the 
left  auricle,  described  by  King,*  sudden  dyspnoea,  cough, 
and  cyanosis  supervened,  and  death  took  place  in  fifteen 
minutes.  In  another  case,  described  by  Ewart,f  no 
symptoms  were  traceable  to  the  perforation. 

A  case  of  rupture  of  an  aneurysm  into  the  right  auricle 
is  also  recorded  by  Ewart,|  and  another  by  Norman  Moore,§ 
in  neither  of  which  were  any  characteristic  symptoms 
present. 

(2)  Aneurysm    of  the  Ascending  Aorta  beyond  the 
Pericardium,  or  Aneurysm  of  Physical  Signs. 

Under  this  head  are  comprised  aneurysms  which  involve 
the  ascending  aorta  between  the  pericardium  and  the  orifice 

*  Transactions  of  the  Pathological  Society,  vol.  26,  p.  37. 

t  Ibid.,  vol.  31,  p.  90.  J  Ibid.,  vol.  31,  p.  95. 

§  Ibid.,  vol.  31,  p.  82 


454 


HEART  DISEASE. 


of  the  innominate  artery.  As  has  already  been  stated,  the 
name,  "aneurysm  of  physical  signs,"  has  been  given  to 
aneurysms  affecting  this  part  of  the  aorta,  since,  from  the 
nature  of  its  anatomical  relations,  pressure  symptoms  do  not 
readily  arise,  and  frequently  the  first  definite  indication  of 
the  existence  of  an  aneurysm  is  the  appearance  of  an  area 
of  pulsation  on  the  chest  wall,  usually  in  the  second  left 


FIG.  3G. — ANEURYSM    OF   ASCENDING   AORTA   WHICH   RUPTURED   INTO   RIGHT 
PLEURAL   CAVITY    AT   A. 

intercostal  space.  Dulness  or  impaired  resonance  on  per- 
cussion may  be  present  before  pulsation  is  visible,  but 
dulness  alone  is  not  sufficient  evidence  of  aneurysm,  and 
pulsation  may  sometimes  be  recognizable  in  the  second  and 
third  left  intercostal  spaces  close  to  the  sternum,  when  the 
aorta  is  dilated  as  in  aortic  incompetence.  When  pulsation 
is  present,  a  diastolic  shock  may  sometimes  be  felt  on 
palpation  over  the  tumour,  and  on  auscultation  the  second 
sound  is  usually  ringing  in  character  and  low  pitched. 

If  the  sac  extends  outwards,  there  will  be  evidence  of 


ANEURYSM  OF  THE  ASCENDING  AORTA.  455 

pressure  on  the  superior  vena  cava,  shown  by  distension 
and  fulness  of  the  veins  on  both  sides  of  the  neck  ;  if  it 
extends  backwards,  there  may  be  symptoms  of  pressure  on 
the  root  of  the  right  lung. 

Pain  in  the  neighbourhood  of  the  aneurysm  is  usually 
present  in  varying  degree,  being  most  severe,  as  a  rule, 
when  the  tumour  is  being  pressed  up  against  the  chest  wall 
and  is  beginning  to  erode  the  ribs. 

An  aneurysm  in  this  situation  may  attain  very  great 
size,  sometimes  being  as  large  as  a  child's  head.  Usually 
it  enlarges  in  the  direction  of  the  blood  current,  that  is, 
towards  the  wall  of  the  thorax,  on  reaching  which  it  may 
erode  the  overlying  ribs,  and  gradually  force  its  way 
through  them  as  they  undergo  atrophy  from  the  pressure. 
It  may  rupture  at  any  stage,  sometimes  into  the  right 
pleural  cavity  (vide  Fig.  36). 

It  may  also  rupture  into  the  lung,  giving  rise  to 
haemoptysis,  which  may  be  profuse  and  terminate  fatally. 
If  the  perforation  is  small  or  at  the  base  of  a  sacculus, 
it  may  become  occluded  by  clot  and  the  haemorrhage  be 
arrested,  but  attacks  of  haemoptysis  are  liable  to  recur  from 
time  to  time  as  the  clot  is  dislodged.  Sometimes  the 
perforation  is  permanently  closed  by  the  development  of 
adhesions.  Frequently  the  lung  tissue  is  compressed  and 
adherent  to  the  sac  of  the  aneurysm,  so  that  when  a  per- 
foration occurs  there  may  be  little  leakage  at  first.  In  one 
case,  from  which  I  put  up  a  specimen  for  the  St.  Mary's 
Hospital  Museum,  there  were  no  less  than  three  separate 
perforations,  and  there  was  a  history  of  recurrent  attacks 
of  haemoptysis  at  intervals  for  over  two  years. 

The  patient  was  a  man  aged  59.  The  first  attack  of 
haemoptysis  occurred  in  December,  1900,  the  next  in 
April,  1902,  a  third  in  September,  a  fourth  in  October, 
the  patient  dying  in  November,  1902.  In  the  third  attack 
10  ozs.,  and  in  the  fourth  20  ozs.  of  blood  were  coughed 


456  HEART  DISEASE. 

up.  At  the  autopsy  there  was  a  large  aneurysm  involving 
the  whole  of  the  arch  of  the  aorta,  spreading  out  in  a  fan- 
like shape.  There  were  two  perforations  on  the  outer 
aspect  of  the  ascending  part  of  the  arch  into  the  right 
lung,  which  were  occluded  by  layers  of  laminated  clot. 
The  adjacent  lung  tissue  was  compressed,  and  adherent  to 
the  sac  of  the  aneurysm  over  the  bases  of  the  perforations, 
which  it  helped  to  seal  up.  The  perforations  were  about 
one-third  of  an  inch  in  diameter.  On  the  outer  aspect  of  the 
descending  portion  of  the  arch  was  a  third  perforation  into 
the  left  lung,  which  was  engorged  with  blood,  and  it  ap- 
peared that  the  recent  attacks  of  haemoptysis  were  due  to 
leakage  from  this  source. 

Aneurysm  of  the  ascending  aorta  is,  however,  compatible 
with  life  for  a  considerable  number  of  years,  as  the  cases 
appended  will  show. 

Case  1. — Harriet  H.,  aged  46,  was  admitted  to  St.  Mary's  Hospital 
in  May,  1887,  with  the  history  that  three  years  before  she  had  noticed 
a  small  lump  in  the  upper  part  of  the  right  side  of  the  chest.  For  a 
year  previous  to  this  she  had  felt  pain  in  the  chest  of  varying  severity. 

On  admission,  there  was  a  small  pulsating  tumour  about  the  size  of 
a  hen's  egg  just  below  the  inner  end  of  the  clavicle  immediately  to  the 
right  of  the  manubrium. 

The  aneurysm  had  already  made  its  way  through  the  chest  wall  by 
erosion  of  the  upper  right  costal  cartilages,  and  was  partially  outside 
the  thoracic  cavity.  There  were  some  enlarged  veins  on  the  front  of 
the  chest  wall,  but  the  jugular  veins  were  not  markedly  distended. 
Thei'e  was  no  evidence  of  pressure  on  the  air  passages,  or  the  recurrent 
laryngeal  nerve.  The  second  sound  was  accentuated  and  somewhat 
low  pitched,  but  was  not  ringing  in  character  or  typical  of  aneurysm. 
After  some  weeks,  she  left  the  hospital,  and  was  readmitted  again  in 
1891,  when  the  aneurysm  had  increased  considerably  in  size,  but  she 
did  not  remain  long  in  hospital.  In  September,  1892,  she  was  again 
admitted.  The  aneurysm  had  then  attained  an  enormous  size,  reaching 
upwards  above  the  clavicle,  and  merging  below  the  right  mamma  into 
a  mass  of  dilated  veins.  The  tumour  was  now  firm  and  resistant,  and 
the  pulsation  was  scarcely  perceptible,  showing  that  a  large  amount  of 
laminated  clot  had  been  deposited  within  the  sac  :  there  was  no  diastolic 
shock.  The  radial  pulse  on  both  sides  was  greatly  modified,  and  the 
right  was  smaller  than  the  left. 

The  jugulars  on  both  sides  were  much  distended,  and  did  not  empty 


ANEURYSM  OF  THE  ASCENDING  AORTA.  457 

on  deep  inspiration.  The  current  of  blood  in  the  dilated  veins  was 
downwards,,  and  they  apparently  anastomosed  with  the  superficial  epi- 
gastric and  intercostal  veins,  showing  that  the  vena  cava  superior  was 
obstructed  by  pressure  of  the  aneurysm,  and  that  some  of  the  blood 
normally  returned  by  the  superior  vena  cava  was  finding  its  way  back 
to  the  heart  by  a  devious  route  through  the  vena  cava  inferior.  A 
photograph  of  this  patient  is  given  (Fig.  35). 

The  tumour  measured  7  inches  across,  9  inches  long,  and  was  about 
19  inches  in  circumference. 

She  remained  in  hospital  six  months,  and  died  at  home  eighteen 
months  later.  Unfortunately,  an  autopsy  was  not  obtainable,  but  it 
was  ascertained  that  she  had  not  died  suddenly  ;  that  is,  from  rupture 
of  the  aneurysm,  but  from  some  intercurrent  pulmonary  complication. 
She  had  thus  survived  nine  or  ten  years  from  the  first  appearance  of 
the  aneurysm. 

Case  2. — Lydia  W.,  aged  40,  first  came  under  observation  at 
St.  Mary's  Hospital  about  fifteen  years  ago.  When  first  admitted,  the 
aneurysm  was  so  small  that  the  diagnosis  was  difficult,  more  especially 
as  she  was  also  suifering  from  aortic  incompetence  in  slight  degree. 
Pulsation  on  the  surface  of  the  chest  wall  was  not  visible,  but  could  be 
made  out  on  firm  palpation  in  the  second  and  third  right  intercostal 
spaces.  The  aortic  second  sound  was,  however,  low  pitched  and  booming 
in  character,  and  typical  of  aneurysm.  While  she  was  in  hospital,  the 
aneurysm  steadily  advanced,  and  pulsation  soon  became  obvious.  She 
suffered  from  pain  and  respiratory  distress,  and  from  attacks  of  palpita- 
tion and  epistaxis.  Treatment  by  pressure  and  iodide  of  potassium 
failed  to  arrest  the  progress  of  the  aneurysm  at  this  stage,  and  it  was 
found  necessary  to  keep  her  in  hospital  for  eighteen  months  on  account 
of  the  severity  of  the  symptoms. 

The  aneurysm  had  greatly  increased  in  size,  and  at  the  end  of  this 
period  pulsation  was  visible  in  the  second  and  third  spaces  as  far  out  as 
the  anterior  axillary  line  with  a  corresponding  increase  of  dulness  on 
percussion.  The  administration  of  iodide  of  potassium,  which  had  been 
discontinued,  was  now  resumed  in  large  doses,  and  consolidation  rapidly 
took  place.  The  tumour  from  being  expansile  became  firm,  showing 
evidence  of  the  deposition  of  laminated  clot  on  its  inner  surface.  All 
her  symptoms  had  greatly  ameliorated,  and  she  left  comparatively  well. 

The  reasons  for  this  improvement,  in  spite  of  increase  in  the  size  of 
the  aneurysm,  seemed  to  be  the  following :  When  she  came  in,  there 
was  a  small  sac  with  a  relatively  large  orifice  communicating  with  the 
aorta,  so  that  the  current  of  blood  swept  through  it,  distending  it  more 
and  more,  and  not  allowing  of  the  deposition  of  clot  within  the  sac. 
When  she  left,  conditions  had  changed  ;  there  was  now  a  large  sac  with 
a  relatively  small  mouth,  so  that  the  main  current  of  blood  rushed  past 
the  orifice  instead  of  through  the  sac,  and  allowed  of  the  formation  of 
layers  of  laminated  clot  upon  its  walls. 

She  has  come  up  to  the  hospital  from  time  to  time  since,  and  when 


458  HEART  DISEASE. 

last  seen,  in  1905,  slie  said  she  did  not  feel  any  special  inconvenience 
from  the  aneurysm.  There  was  then  a  pulsating  tumour  about  the  size 
of  a  hen's  egg  in  the  second  and  third  right  intercostal  spaces,  not  pro- 
jecting very  much  above  the  surface  of  the  chest  wall.  A  general  heave 
was  communicated  to  the  chest  wall  around  this  area,  and  pulsation 
could  be  felt  by  deep  palpation  in  the  second  and  third  spaces  as  far 
as  the  anterior  axillary  line,  over  which  area  there  was  dulness  on 
percussion. 

On  palpation  over  the  aneurysm,  a  well-marked  diastolic  shock  was 
felt.  The  aortic  second  sound  was  low  pitched  and  ringing,  and  a 
diastolic  murmur  was  also  audible. 

There  was  no  evidence  of  pressure  on  the  superior  vena  cava,  no 
difference  in  the  pulses,  no  affection  of  the  vocal  cords.  The  pulse 
wave  was  forcible  and  sudden  in  character,  but  was  sustained  instead 
of  collapsing,  and  presented  the  characters  of  the  pulse  of  aortic  incom- 
petence scarcely  modified  by  the  aneurysm. 

This  is  practically  a  case  of  cured  aneurysm.  The  walls  of  the  sac 
have  become  thick  and  strong  from  deposit  of  laminated  clot  within 
and  chronic  inflammatory  changes  without,  and  there  is  little  chance 
of  rupture.  She  has  now  survived  fifteen  years  from  the  onset  of 
the  aneurysm,  and  seldom  has  any  symptoms  to  remind  her  of  its 
existence. 


(3)  Aneurysm  op  the  Transverse  Part  of  the  Arch. 
Aneurysm  op  Symptoms. 

The  name,  aneurysm  of  symptoms,  has  been  given  to 
aneurysms  affecting  the  transverse  part  of  the  arch  because, 
as  a  rule,  characteristic  and  important  symptoms  early 
arise  which  engender  a  suspicion  of  aneurysm  some  time 
before  the  physical  signs  are  at  all  demonstrative  of  its 
existence. 

Most  of  the  symptoms  which  may  arise  have  already 
been  enumerated  under  the  head  of  "  Pressure  Symptoms ; " 
but,  for  the  sake  of  clearness,  it  will  be  necessary  to  briefly 
discuss  them  here. 

The  symptoms  will  vary,  and  one  or  other  of  them  will 
present  themselves  according  as  the  aneurysm  is  situated 
in  the  convexity  or  concavity  of  the  arch,  or  upon  its 
anterior  or  posterior  surface. 

1.  Pressure   on  the   Left   Recurrent  Laryngeal  Nerve. — 


ANEURYSM  OF  THE  ARCH  OF  THE  AORTA.  459 

As  this  nerve  winds  round  the  aorta,  an  aneurysm  on  any 
aspect  of  the  aortic  arch  may  press  upon  it  or  stretch  it, 
giving  rise  to  characteristic  symptoms. 

One  of  these  is  the  "  cracked  "  voice,  which  is  so  pecu- 
liar as  to  be  almost  diagnostic. 

Not  infrequently  the  patient  will  come  up  to  the  throat 
department,  or  consult  a  throat  specialist,  complaining  of 
hoarseness  and  alteration  of  voice  ;  or,  if  he  happens  to  have 
a  cough,  he  may  have  also  noticed  that  the  sound  made 
when  he  coughs  has  an  altered,  brassy  character.  There  is 
not,  as  a  rule,  dyspnoea  unless  there  is  in  addition  pressure 
by  the  aneurysm  on  the  trachea  or  one  of  the  bronchi.  On 
examination  of  the  larynx,  it  will  be  found  that  these 
symptoms  are  due  to  paralysis  of  the  left  vocal  cord. 

The  paralysis  that  results  from  pressure  on  the  recurrent 
laryngeal  nerve  is  that  of  the  abductors  of  the  larynx,  so 
that  the  left  vocal  cord  will  be  seen  fixed  and  motionless  in 
the  median  line  in  the  position  of  phonation.  This  may  be 
the  first,  and  the  only  suspicious  symptom  of  aneurysm,  but 
it  is  very  significant  when  present,  as  nothing  except  a 
tumour  pressing  on  the  recurrent  nerve  in  some  part  of  its 
course  can  give  rise  to  one-sided  laryngeal  palsy,  and  of 
such  tumours,  by  far  the  commonest  is  aneurysm.  The 
right  recurrent  laryngeal  nerve  may  be  compressed  by  the 
sac  of  an  aneurysm  involving  the  innominate  artery,  as  is 
illustrated  in  the  second  case  described  later  on. 

2.  Pressure  on  the  Trachea,  (Esophagus,  and  Thoracic  Duct. 
— Symptoms  arising  from  pressure  on  these  structures  may 
be  the  earliest  indications  of  an  aneurysm  on  the  posterior 
surface  of  the  arch,  or  of  a  saccular  aneurysm  extending 
posteriorly. 

Pressure  on  the  trachea  may  give  rise  to  slight  dyspnoea, 
but  this,  as  a  rule,  is  only  marked  when  there  is  in  addition 
paralysis  of  one  of  the  vocal  cords.  Auscultation  of  the 
limo-s   will   show   the   modification   of  the   breath   sounds 


460  HEART  DISEASE. 

known  as  tracheal  breathing.  Rupture  of  the  aneurysm 
into  the  trachea  may  occur  as  illustrated  in  Fig.  37,  and 
give  rise  to  profuse  and  fatal  haemoptysis. 

The  tracheal  tug,  already  described,  will  as  a  rule  be 
recognizable  before  the  pressure  gives  rise  to  dyspnoea. 

Pressure  on  the  oesophagus  will  cause  difficulty  in 
swallowing,  and  it  has  happened  ere  now  that  adventurous 
persons  seeking  to  ascertain  the  cause  of  some  obscure 
oesophageal  obstruction  by  passing  a  bougie,  have  un- 
expectedly done  so  by  passing  it  through  the  sac  of  an 
aortic  aneurysm.  Many  cases  are  on  record  of  spontaneous 
rupture  into  the  oesophagus  with  resulting  profuse  and 
fatal  hseniaternesis. 

Pressure  on  the  thoracic  duct  gives  rise  to  no  very 
definite  symptoms,  but  causes  impairment  of  nutrition  by 
obstructing  the  flow  into  the  general  circulation  of  lymph 
and  products  of  digestion  absorbed  from  the  lacteals. 

Pressure  on  the  ciliospinal  branch  of  the  sympathetic 
may  cause  dilatation  or  contraction  of  the  left  pupil  according 
as  its  fibres  are  irritated  or  destroyed. 

3.  Pressure  on  the  Root  of  the  Left  Lung. — If  the 
aneurysm  is  on  the  concavity  of  the  arch,  or  the  sac  extends 
downwards,  it  may  give  rise  to  symptoms  arising  from 
pressure  on  the  root  of  the  left  lung,  already  described 
above.  The  most  marked  of  these  will  be  diminished  entry 
of  air  on  the  affected  side. 

Difference  between  the  Radial  Pulses. — Difference  between 
the  pulses  is  especially  liable  to  occur  in  aneurysms  in- 
volving this  portion  of  the  aortic  arch,  since  the  innominate 
or  left  sub-clavian  may  be  given  off  from  the  sac  or  be 
compressed  by  it,  or  the  sac  may  be  interposed  between  the 
two  vessels. 

Physical  Signs.  Pulsation. — Usually  some  of  the 
symptoms  above  described  precede  the  appearance  of  pulsa- 
tion on  the  chest  wall.     If  the  aneurysm  is  situated  on  the 


ANEURYSM  OF  THE  ARCH   OF  THE  AORTA. 


461 


posterior  aspect  of  the  arch,  visible  pulsation  may  be  absent 
throughout  the  course  of  the  disease.  More  commonly,  if 
the  aneurysm  attains  any  considerable  size,  it  gives  rise  to 
an  obscure  general  heave  of  the  manubrium  best  appreciated 
by  laying  the  palm  of  the  hand  on  the  part.     When  it 


J   — 


FIG.  37. — ANEURYSM   OF   THE    TRANSVERSE   PART   OP   THE    ARCH   WHICH 
RUPTURED   INTO   THE   TRACHEA   AT   X.       (FRONT   VIEW.) 

springs  from  the  anterior  aspect  of  the  arch,  the  sac  may 
present  as  a  pulsating  tumour  in  the  second  or  third  left 
intercostal  space  close  to  the  margin  of  the  sternum. 
Sometimes  pulsation  in  the  sac  may  be  felt  by  pressing  the 
finger  down  behind  the  sternal  notch,  before  it  is  evident 
on  the  chest  walls,  but  care  must  be  taken  not  to  mistake 
a  dilated  aorta  for  an  aneurysm. 


462  HEART  DISEASE. 

Dulness  on  percussion  over  the  manubrium  sterni,  and 
immediately  to  the  left  of  it,  may  often  be  made  out  before 
pulsation  is  visible,  and  when  occurring  in  conjunction  with 
some  of  the  characteristic  symptoms,  is  a  valuable  sign, 
though  the  possibility  of  its  being  due  to  enlarged  glands 
or  other  mediastinal  tumour,  must  be  borne  in  mind. 

On  auscultation,  tracheal  breathing  may  sometimes  be 
heard  over  the  manubrium,  conducted  by  an  aneurysm  in 
contact  posteriorly  with  the  trachea  and  anteriorly  with  the 
chest  wall. 

The  aortic  second  sound  may  be  reinforced,  that  is,  may 
be  louder  and  more  distinct  to  the  left  of  the  manubrium 
than  in  the  normal  situation,  and  occasionally  may  be 
audible  in  the  left  supra-scapular  space. 

A  systolic  murmur  is  sometimes  heard  over  the  course  of 
the  aortic  arch  to  the  left  of  the  manubrium,  though  no 
murmur  is  audible  in  the  aortic  area. 

Course  of  the  Disease. — -An  aneurysm  in  this  situation  on 
account  of  the  important  structures  in  immediate  relation 
with  it  usually  gives  rise  at  an  early  stage  to  one  or  other 
of  the  symptoms  enumerated  above.  It  is  only  when  it  is 
situated  on  the  upper  and  anterior  aspect  of  the  arch,  and 
attains  a  considerable  size,  that  physical  signs  such  as 
dulness  over  the  manubrium  sterni,  and  to  the  left  of  it, 
or  pulsation  in  the  second  left  intercostal  space  may  precede 
the  appearance  of  symptoms.  It  never  attains  the  great 
size  sometimes  seen  in  aneurysms  of  the  ascending  aorta, 
and  usually  proves  fatal  at  a  much  earlier  period. 

If  it  is  situated  posteriorly  and  extends  backwards,  it 
may  ulcerate  through  the  trachea,  and  rupture  into  it 
when  quite  small,  as  seen  in  Figs.  37  and  38. 

In  this  case  the  aneurysm  was  situated  on  the  posterior 
aspect  of  the  arch,  and  was  only  about  the  size  of  a  plover's 
egg  when  it  ruptured  into  the  trachea. 

It   may    ulcerate    through  and    rupture   into  the    left 


ANEURYSM  OF  THE  ARCH  OF  THE  AORTA. 


46- 


bronchus  or  the  oesophagus,  or  it  may  rupture  into  the  left 
pleural  cavity,  left  lung,  or  posterior  mediastinum. 

Death  may  occur  from  pulmonary  complications  caused 
by  pressure  on  the  trachea  or  root  of  left  lung. 

The  two  following  cases  illustrate  the  predominance  of 


a.  Sac  of  aneurysm  ;    b.  Innominate  artery ;   c.  Left  carotid  ;  d.  Left 
sub-clavian. 


FIG.  38.- 


-ANEURYSM   OP   TRANSVERSE   PART   OP   THE   ARCH   WHICH   RUPTURED 
INTO   THE   TRACHEA.      (SIDE   VIEW,   SHOWING   SAC.) 


synrptorns  over  physical  signs  in  the  early  stages  of  the 
disease,  and  the  rapidity  with  which  it  may  progress  and 
cause  death  from  pressure  on  the  respiratory  passages  and 
other  important  structures.  They  are  also  especially 
interesting,  clinically,  from  the  number  and  variety  of 
symptoms  and  physical  signs  which  developed  during  the 


464  HEART  DISEASE. 

course  of  the  disease.  In  the  second  of  these  two  cases 
the  right  vocal  cord  was  paralyzed,  as  the  right  sub-clavian 
artery  was  embedded  in  the  sac  of  the  aneurysm  which 
had  involved  the  orifice  of  the  innominate  artery. 

Cask  1. — The  patient,  a  strong-looking-,  well-nourished  man,  aged 
54;  was  admitted  to  St.  Mary's  Hospital  in  November,  1894,  complaining 
of  cough  and  shortness  of  breath  ;  his  lips  were  rather  blue,  and  his 
face  was  congested.  His  chest  was  somewhat  barrel-shaped,  and  the 
cardiac  dulness  was  masked  by  emphysema  :  rhonchi  were  audible  over 
both  lungs.  At  first  sight  the  case  looked  like  one  of  simple  emphysema 
and  bronchitis.  On  careful  observation  it  was  noticed  that  the  left 
external  jugular  vein  was  much  more  distended  than  the  right,  and 
did  not  empty  on  deep  inspiration  ;  the  veins  in  the  left  arm  were  full 
and  distended,  and  a  large  tortuous  vein  was  also  visible  running  across 
the  front  of  the  left  shoulder,  from  the  external  jugular  to  the  cephalic 
vein,  in  which  the  current  of  blood  was  downwards. 

The  carotid  artery  on  the  left  side  was  difficult  to  see,  and  pulsation 
in  it  could  scarcely  be  detected  ;  in  the  right  carotid  pulsation  could  be 
seen  and  felt  without  difficulty. 

The  pupils  were  unequal  in  size,  the  left  being  larger  than  the  right. 

The  left  side  of  the  chest  was  noticed  not  to  move  so  well  in  respira- 
tion as  the  right,  and  on  auscultation  the  entry  of  air  was  not  so  good. 
The  percussion  note  was  good  on  both  sides.  Tracheal  breathing  could 
be  heard  over  the  manubrium,  and  for  a  short  distance  on  either  side 
of  it. 

These  indications  seemed  to  point  to  a  tumour  which  pressed  on  the 
trachea  and  left  bronchus,  compressed  the  left  innominate  vein  hinder- 
ing the  return  of  blood  through  it  to  the  heart,  interfered  with  the  flow 
of  blood  through  the  left  carotid,  and  also  stimulated  a  branch  of  the 
sympathetic,  causing  dilatation  of  the  left  pupil. 

A  tumour  which  would  do  this  could  scarcely  be  anything  else  than 
an  aneurysm  of  the  aorta.  In  support  of  this,  it  was  found  that  there 
was  marked  tracheal  tugging.  There  was,  however,  no  difference  in 
the  radial  pulses,  no  affection  of  the  vocal  cords,  and  there  was  no  area 
of  pulsation  to  be  detected  on  the  chest  wall.  At  the  end  of  five  weeks, 
slight  pulsation  could  be  made  out  in  the  second  left  intercostal  space 
at  the  end  of  expiration,  and  there  was  a  small  area  of  dulness  to  the 
left  of  the  manubrium. 

While  the  patient  was  under  observation,  the  left  pupil  was  seen 
to  alter  frequently  in  size,  being  sometimes  smaller,  sometimes  larger 
than  the  right. 

Rest  and  treatment  failed  to  improve  his  condition,  and  on  January 
17th,  seven  weeks  after  admission,  he  had  a  severe  attack  of  dyspnoea, 
sweating  profusely,  and  becoming  cyanosed.  He  was  bled  ten  ounces 
from  the  arm,  which  relieved  him  considerably  for  a  time. 


ANEURYSM  OF  THE  ARCH  OF  THE  AORTA.  465 

Six  days  later  he  had  another  similar  but  more  severe  attack  of 
dyspnoea,  and  this  time  inspiration  was  harsh  and  crowing,  as  if  there 
was  some  laryngeal  spasm,  so  that  tracheotomy  was  contemplated,  but 
was  not  deemed  advisable.  Venesection  gave  no  relief,  but  inhalation 
of  chloroform  stopped  the  laryngeal  stridor.  He  had  several  attacks 
of  dyspnoea  during  the  day,  and  became  much  exhausted.  He  died 
suddenly  in  the  evening. 

At  the  autopsy,  an  aneurysm  about  the  size  of  a  small  cocoa-nut 
was  found  at  the  upper  and  posterior  aspect  of  the  transverse  part  of 
the  arch  where  it  crossed  the  trachea.  The  trachea  at  its  bifurcation, 
and  the  left  bronchus  were  compressed  by  the  tumour,  and  the  oeso- 
phagus was  displaced  to  the  left. 

The  left  innominate  vein  was  stretched  over  the  sac,  and  its  lumen 
was  almost  obliterated.  A  portion  of  the  aneurysmal  sac  extended  up 
behind  the  left  common  carotid  artery,  which  was  flattened  and  com- 
pressed by  it. 

The  left  sub-clavian  artery  was  not  involved  in  the  aneurysm. 

Case  2. — Aneurysm  affecting  the  anterior  portion  of  the  transverse 
part  of  the  arch  close  to  the  origin  of  the  innominate  artery. 

Samuel  B ,  age  27.  This  patient  came  to  the  Throat  Depart- 
ment of  St.  Mary's  Hospital  complaining  of  hoarseness  and  attacks  of 
difficulty  in  breathing.  On  examination  of  the  larynx,  it  was  found 
that  the  right  vocal  cord  was  paralyzed  :  aneurysm  being  suspected,  he 
was  sent  up  to  the  wards.  On  admission,  his  dyspnoea  was  very  severe, 
his  face  was  flushed  and  swollen,  and  when  he  was  able  to  speak,  his 
voice  was  noticed  to  be  cracked  and  hoarse,  and  his  inspiration  was 
wheezing.  He  stated  that  he  had  been  quite  well  till  about  six  weeks 
previously,  when  he  had  a  sudden  attack  of  difficulty  in  breathing, 
which  was  considered  to  be  croup  and  was  treated  as  such.  He  also 
complained  of  a  troublesome  cough  and  difficulty  in  swallowing. 

On  inspection  of  the  chest,  on  both  sides  large  veins  were  seen  over 
the  front,  in  which  the  current  of  blood  was  downwards,  carrying  blood 
from  the  veins  of  the  neck  to  the  intercostal  veins.  The  external 
jugulars  on  both  sides  were  full  and  distended  ;  and  it  was  evident  that 
the  vena  cava  superior  was  occluded  by  pressure. 

The  pulse  was  absent  in  the  right  wrist,  and  in  the  right  sub-clavian 
and  carotid. 

Examination  of  the  chest  showed  dulness  on  percussion  over  the 
manubrium,  and  to  the  right  and  left  of  it  for  a  short  distance. 

There  was  diffuse  but  faint  pulsation  over  this  region,  best  felt  in 
expiration,  and  a  loud  ringing  second  sound  was  audible. 

Over  the  front  of  the  right  lung  there  was  absence  of  respiratory 
murmur  and  of  vocal  resonance,  with  normal  resonance  on  percussion, 
a  condition  which  was  clearly  due  to  pressure  on  the  root  of  the  lung. 
Posteriorly  in  the  suprascapular  region  tubular  breathing  could  be 
heard  on  both  sides  ;  over  the  bases  the  entry  of  air  was  good. 

The  pupils  were  unequal,  the  right  being  smaller  than  the  left. 

2h 


466  HEART  DISEASE. 

This  was  his  condition  on  admission.  He  got  gradually  worse.,  in 
spite  of  rest  in  bed  and  treatment.  Iodide  of  potash;,  ergot,  and  opium 
were  administered  ;  venesection  was  practised  for  the  relief  of  pain,  and 
was  effectual  at  the  time,  but  the  relief  only  lasted  two  or  three  days. 
He  died  suddenly  two  months  after  admission. 

At  the  autopsy  an  aneurysm  the  size  of  a  large  fist  was  found  spring- 
ing from  the  anterior  wall  of  the  arch,  close  to  the  origin  of  the  in- 
nominate. The  communication  between  the  aneurysmal  sac  and  the 
aorta  was  about  the  size  of  a  shilling.  The  origin  of  the  innominate 
artery  was  involved  in  the  sac,  and  was  not  recognizable ;  the  right 
sub-clavian  was  patent  but  small,  it  ran  up  the  posterior  wall  of  the  sac, 
arising  from  it  by  a  valvular  opening.  The  right  carotid  contained  a 
plug  of  coagulated  fibrin,  but  there  was  a  small  passage  by  the  side  of 
the  clot.  The  left  carotid  and  sub-clavian  came  off  beyond  the  sac  and 
were  not  interfered  with. 

The  vena  cava  superior  was  flattened  out  on  the  front  of  the  sac, 
and  was  discoverable  with  difficulty,  but  it  was  not  completely  oblite- 
rated :  the  right  innominate  vein  was  quite  destroyed  ;  the  left  was 
flattened  out,  but  the  lumen  was  not  entirely  obliterated. 

The  trachea  was  compressed  by  the  tumour,  as  were  also  the  bronchi 
leading  to  the  upper  lobes  of  both  lungs,  more  especially  on  the  right 
side.  The  mucous  membrane  of  the  trachea  was  ulcerated.  The  oeso- 
phagus was  also  indirectly  pressed  upon,  the  trachea  intervening  between 
it  and  the  sac.  The  right  recurrent  laryngeal  nerve  was  compressed, 
and  also  the  right  vagus,  which  was  involved  in  the  adhesions  round 
the  aneurysmal  sac. 

Here  the  symptoms  caused  by  the  pressure  effects  of  the 
aneurysm  on  the  important  structures  surrounding  it, 
occupied  a  more  prominent  position  in  the  history  of  the 
case  than  the  presence  of  abnormal  pulsation  on  the  chest 
wall,  which  was  at  no  time  well  marked.  The  first  symptoms 
were  laryngeal,  caused  by  pressure  of  the  aneurysm  on  the 
right  recurrent  laryngeal  nerve.  The  presence  of  the 
abnormal  veins  on  the  chest  wall,  and  the  absence  of 
pulsation  in  the  right  carotid  and  radial  vessels  were 
striking  features.  The  full  jugulars,  the  distended  veins  on 
the  front  of  the  chest  in  which  the  current  of  blood  was 
found  to  be  downwards,  pointed  to  some  obstruction  of  the 
superior  vena  cava,  and  these  phenomena,  together  with 
the  paralysis  of  the  right  vocal  cord,  and  disturbance 
of  circulation  in  the  rio;ht  carotid  and  radial,  would  have 


ANEURYSM  OF  THE  DESCENDING  AORTA.  467 

been  sufficient,  even  in  the  absence  of  pulsation  on  the 
chest  wall,  to  enable  one  to  come  to  a  diagnosis  of 
aneurysm. 


(4)  Aneurysms  op  the  Third  or  Descending  Part  of 

the  Arch. 

The  descending  aorta  is  deeply  seated,  lying  to  the  left 
side  of  the  bodies  of  the  fourth  and  fifth  dorsal  vertebrae. 
The  only  important  structures  in  immediate  relation  are 
the  oesophagus  and  thoracic  duct,  which  lie  to  the  right  of 
the  aorta.  Pressure  symptoms  are  consequently  not,  as  a 
rule,  characteristic,  and  as  the  aneurysm  rarely  comes  to 
the  surface,  physical  signs  are  usually  ill-marked.  There 
may,  however,  be  dysphagia  from  pressure  on  the  oesophagus, 
and  a  not  uncommon  termination  is  rupture  of  the  aneurysm 
into  the  oesophagus.  Frequently  the  only  symptom  com- 
plained of  is  pain  in  the  back,  a  pain  radiating  down  the 
left  arm  or  round  the  left  side  of  the  chest :  there  may 
be  no  other  physical  signs  or  symptoms  present.  The  pain 
is  due  either  to  irritation  of  a  spinal  nerve,  when  it  may 
radiate  round  the  left  side  of  the  chest,  or  to  erosion  of 
the  vertebrae,  when  smartly  tapping  the  affected  vertebra 
sometimes  increases  the  pain.  Diagnosis  is  in  most  cases  a 
matter  of  considerable  difficulty. 

The  aneurysmal  sac  may,  however,  enlarge  in  such  a 
direction  as  to  press  on  the  root  of  the  left  lung  and  the 
recurrent  laryngeal  nerve.  In  one  case,  where  the  patient  had 
been  sent  to  the  hospital  for  chronic  laryngitis  and  attacks 
of  paroxysmal  dyspnoea,  the  left  vocal  cord  was  found  to  be 
paralyzed,  and  there  were  signs  of  pressure  on  the  left 
bronchus,  which  seemed  to  point  to  aneurysm  of  the  trans- 
verse part  of  the  arch.  At  the  autopsy,  however,  an 
aneurysm  was  found  involving  the  aorta  to  the  left  of  the 
bodies  of  the  fourth  and  fifth  dorsal  vertebrae  and  adherent 


468  HEAR!   DISEASE. 

to  thein,  and  to  the  lower  part  of  the  body  of  the  third 
dorsal  vertebra. 

In  the  accompanying  illustration  (Fig.  39),  a  large 
aneurysm  of  the  descending  aorta  is  shown,  which  compresses 
the  oesophagus,  and  is  adherent  to  the  dorsal  vertebrae 
from  the  fourth  to  the  eighth. 

Diagnosis. 

Little  need  be  said  here  under  this  head,  as  the 
symptoms  and  physical  signs  characteristic  of  aneurysm 
have  been  fully  discussed.  It  must,  however,  be  borne  in 
mind  that  a  solid  tumour  in  the  mediastinum,  such  as  a 
malignant  growth,  or  enlarged  mediastinal  glands,  may 
give  rise  to  many  of  the  pressure  symptoms  produced  by 
aneurysm.  Any  mediastinal  tumour  may  compress  the 
great  veins,  the  trachea,  cesophagus,  thoracic  duct,  the  root 
of  the  lung,  or  may  even  involve  the  recurrent  laryngeal 
nerve  or  sympathetic.  In  conjunction  with  symptoms  pro- 
duced by  pressure  on  one  or  other  of  these  structures,  there 
may  be  an  area  of  dulness  over,  and  to  one  or  both  sides  of 
the  manubrium  sterni.  Pulsation  will,  as  a  rule,  be  absent, 
and  there  will  not  be  the  modification  of  the  aortic  second 
sound  which  is  common  in  aneurysm.  Oases  may  neverthe- 
less occur  in  which  pulsation  is  communicated  from  the 
arch  of  the  aorta  to  a  tumour  intervening  between  it  and 
the  chest  wall,  and  there  is  a  diffuse  general  heave  of  the 
upper  part  of  the  thorax.  If,  on  palpation,  a  diastolic 
shock  is  felt,  all  uncertainty  will  be  at  an  end,  as  this 
could  only  be  present  in  aneurysm. 

On  pressing  the  fingers  down  into  the  intercostal  spaces 
a  sense  of  resistance  will  be  imparted  by  a  solid  tumour, 
and  no  true  expansile  pulsation  will  be  felt.  An  aneurysm 
will  sooner  or  later  tend  to  present  as  a  pulsatile  swelling 
in  one  of  the  intercostal  spaces,  while  the  growth  of  a  solid 


ANEURYSM  OF  THE  DESCENDING  AORTA. 


469 


tumour  will  be  indicated  only  by  extension  of  dulness  on 
percussion,  without  extension  or  localization  of  pulsation. 
The  history  of  the  onset  of  the  disease  will  be  of  service, 


FIG.    39. — ANEURYSM   OF   DESCENDING   AORTA. 


and  usually  careful  observation  of  the  progress  of  the  case 
will  soon  clear  up  all  doubt. 

It  will  be  seen  that  a  tumour  in  the  mediastinum  is 
most  likely  to  be  confused  with  aneurysm  of  the  transverse 
part  of  the  arch. 


47o  HEART  DISEASE. 

Aneurysm  of  the  descending  aorta  may  closely  simulate 
spinal  caries,  when  it  compresses  the  spinal  nerves  and 
begins  to  erode  the  bodies  of  the  vertebrae,  and,  as  has 
already  been  stated,  pain  may  be  the  only  symptom  to 
which  it  gives  rise.  The  absence  of  rigidity  of  the  spine 
will  usually  serve  to  exclude  spinal  caries,  but  the  cause 
of  the  pain  may  be  difficult  to  ascertain.  If  dysphagia  is 
present  in  addition,  this  will  be  a  help  to  diagnosis,  but 
it  may  be  impossible  to  diagnose  with  any  certainty  the 
existence  of  an  aneurysm  of  the  descending  aorta,  or  that 
of  an  intra-pericardial  aneurysm. 

In  doubtful  cases  an  X-ray  screen  or  photograph  may 
be  of  great  service. 

Prognosis. 

The  prognosis  varies  according  to  the  situation  of  the 
aneurysm  and  the  direction  in  which  it  extends,  according 
to  its  shape,  whether  fusiform  or  sacculated,  according  as 
it  increases  rapidly  or  slowly  in  size. 

When  situated  in .  the  intra-pericardial  portion  of  the 
aorta,  it  usually  proves  fatal  by  sudden  rupture  before  it 
attains  any  considerable  size.  The  vessel  at  this  part  lying 
free  in  the  pericardial  sac,  there  are  no  surrounding  struc- 
tures which  the  aneurysm  can  appropriate  for  its  support, 
and  there  is  also  considerable  up-and-down  movement  of 
the  rest  of  the  aorta.  These  conditions  favour  rapid  extension 
and  rupture  of  the  aneurysm. 

As  the  physical  signs  and  symptoms  are  so  indefinite,  it 
is  difficult  to  make  an  early  or  certain  diagnosis,  but  where 
evidence  points  to  the  presence  of  an  aneurysm  in  this 
situation,  the  condition  of  the  patient  is  one  of  imminent 
danger,  and  little  can  be  done  to  arrest  the  progress  of  the 
aneurysm. 

When  situated  in  the  ascending  portion  of  the  arch 
above    the    pericardium,    the    aneurysm    may    attain    an 


PROGNOSIS  IN  ANEURYSM.  47 1 

enormous  size,  and  the  patient  live  for  some  years  without 
experiencing  much  inconvenience  from  it,  especially  if  the 
aneurysm  extends  forwards,  and  makes  its  way  through  the 
chest  wall.  While  the  aneurysm  is  eroding  the  chest  wall 
and  making  its  way  through,  there  may  be  considerable 
pain  which  will  disappear  later,  but,  the  resistance  offered 
by  the  chest  wall  in  front  being  overcome,  the  pressure 
on  deep-seated  parts  will  be  diminished. 

If  the  aneurysm  extends  backwards,  the  prognosis  is  less 
favourable,  as  serious  complications  may  arise  from  pressure 
on  the  root  of  the  lung  or  the  vena  cava,  or  perhaps  on  the 
pneumogastric  nerve. 

When  it  involves  the  transverse  portion  of  the  arch,  to 
the  danger  of  the  aneurysm  per  sc  must  be  added  the 
danger  of  pressure  effects  on  the  important  structures  in  its 
neighbourhood.  Death  may  occur  suddenly  from  rupture 
into  the  trachea  or  elsewhere,  or,  more  slowly,  from  asphyxia 
and  pulmonary  collapse  due  to  pressure  on  the  trachea  or 
on  the  root  of  one  or  other  lung.  If,  however,  the  aneu- 
rysm extends  forwards  instead  of  backwards,  and  comes 
to  the  surface  of  the  chest  wall,  the  prognosis  is  less  un- 
favourable. 

With  regard  to  the  shape  of  the  aneurysm,  if  it  is  of 
the  sacculated  variety,  it  may  extend  rapidly  at  first,  and 
perhaps  prove  fatal  by  rupture  at  an  early  period ;  as  it 
continues  to  enlarge,  however,  the  mouth  of  the  sac  will 
become  relatively  small  compared  with  the  size  of  the 
tumour :  thus  less  blood  enters  the  sac,  and  the  circulation 
in  it  is  slowed.  These  conditions  favour  the  deposition  of 
fibrin,  so  that  the  progress  of  the  aneurysm  may  be  checked, 
or  a  spontaneous  cure  result.  In  fusiform  aneurysm  the 
progress  of  the  aneurysm  is  usually  slow ;  but  little  can 
be  done  to  arrest  it,  as  the  blood  sweeping  through  the 
whole  of  the  sac  gives  little  chance  for  the  deposition  of 
fibrin  on  its  walls,  and  washes  it  away  when  deposited. 


472  HEART  DISEASE. 


Tkeatment. 


Iii  the  treatment  of  aortic  aneurysm  the  object  to  be 
attained  is  to  keep  down  the  blood  pressure,  to  render  the 
circulation  as  slow  and  equable  as  possible,  to  diminish  the 
volume  of  blood,  and  to  increase  its  coagulability.  We 
shall  thus  reduce  the  strain  on  the  walls  of  the  aneurysm 
to  a  minimum,  and  favour  the  coagulation  of  blood  in  the 
sac.  For  this  purpose  the  most  important  measure  is  rest ; 
the  patient  should  be  kept  in  bed  for  six  weeks  or  two 
months.  It  may  be  necessary  to  allow  him  to  use  a  commode 
when  the  bowels  act,  as  the  straining  attending  the  use  of 
the  bed  pan  may  give  rise  to  more  effort  than  sitting  up, 
but  he  should  not  get  out  of  bed  for  any  other  purpose. 
Excitement  of  any  kind  must  be  avoided.  Next  in  impor- 
tance to  rest  is  feeding.  The  amount  of  liquid  taken  with 
meals  should  be  reduced  to  a  minimum,  40  or,  if  practicable, 
30  ounces  only  being  taken  in  the  24  hours.  Soups,  game, 
salt  fish,  rich  sauces,  beer,  and  tea  should  be  forbidden,  and 
meat  should  be  used  in  moderation,  as  extractives,  rich 
foods,  and  excess  of  nitrogenous  matter  may  lead  to  the 
retention  of  toxic  materials  in  the  blood,  which  give  rise 
to  increase  in  the  peripheral  resistance  by  their  vaso- 
constrictor action.  The  food  should  not  be  bulky,  that  is, 
should  not  include  too  much  farinaceous  matter,  such  as 
potatoes,  rice,  etc. ;  the  amount  of  food  taken  at  each  meal 
should  be  about  the  same,  and  should  not  be  excessive,  so 
as  to  avoid  the  extremes  of  repletion  or  depletion,  and  the 
varying  rapidity  of  the  circulation  which  would  result  were 
some  meals  copious  and  others  small.  The  reduction  of 
the  volume  of  blood  favours  the  repair  of  aneurysm  in  two 
ways — it  lessens  the  distension  of  the  entire  vascular  system, 
and  therefore  the  internal  pressure  in  the  sac,  and  the  rate 
of  flow  of  blood  is  diminished ;  further,  the  blood  being 
inspissated,  fibrin  is  more  readily  deposited. 


TREATMENT.  473 

There  is  one  drug  which  undoubtedly  has  a  favourable 
influence  on  aneurysm,  namely,  iodide  of  potassium.  This 
should  be  given  in  gradually  increasing  doses,  till  20,  30, 
or  40  grains  are  taken  three  times  a  day.  Its  precise  mode 
of  action  has  been  much  discussed ;  chemically  it  has  a 
solvent  influence  on  fibrin,  and  cannot  therefore  be  supposed 
to  favour  its  precipitation  on  the  wall  of  the  sac ;  neither 
can  the  good  effects  of  this  drug  in  aneurysm  be  ascribed 
to  its  action  on  the  aneurysm  as  a  remote  effect  of  syphilis. 
It  is  probable  that  it  co-operates  with  the  rest  and  diet, 
firstly,  by  its  depressing  influence  on  the  action  of  the 
heart ;  secondly,  by  promoting  diuresis,  and  thus  helping 
to  drain  off  water  and  inspissate  the  blood. 

•  Aperients  may  have  to  be  taken  to  obviate  constipation, 
which  would  have  a  very  injurious  influence,  and  it  may 
be  necessary  to  counteract  restlessness  and  assist  sleep  by 
bromides  or  opiates.  Morphia  may  also  be  required  for  the 
relief  of  pain. 

Sibson  gave  ergot  in  large  doses  in  cases  of  aneurysm, 
and  it  could  be  easily  demonstrated  that  the  pulsation 
diminished  in  an  aneurysm  which  had  perforated  the  chest 
wall,  and  that  its  volume  was  lessened.  This  he  attributed 
to  the  contraction  of  muscular  fibres  in  the  wall  of  the 
sac,  but  such  fibres  are  non-existent.  The  cause  was  un- 
doubtedly diminished  output  of  blood  by  the  left  ventricle, 
due  to  limitation  of  its  diastole  by  the  ergot. 

Venesection  may  be  of  the  greatest  service  when  there  is 
severe  pain.  It  usually  affords  immediate  relief  by  lowering 
the  tension  within  the  aneurysm,  and  it  may  also  so  lessen 
the  amount  of  blood  in  circulation  as  to  afford  a  chance  of 
fibrin  being  deposited.  Surgery  does  not  find  much  oppor- 
tunity in  the  treatment  of  thoracic  aneurysm,  but  ligature 
of  the  right  sub-clavian  and  carotid  arteries  when  the  in- 
nominate is  involved,  or  of  the  corresponding  vessels  on  the 
left  side  when  the  origins  of  the  left  carotid  and  sub-clavian 


474  HEART  DISEASE. 

were  implicated,  has,  in  some  instances,  led  to  consoli- 
dation of  the  sac,  by  reducing  the  flow  of  blood  through 
it.  Other  expedients  have  been  tried,  such  as  the  intro- 
duction of  coils  of  fine  wire  into  the  sac,  passed  in  through 
a  trocar,  or  the  action  of  galvanic  currents,  with  the  object 
of  the  formation  of  a  coagulum  in  the  sac,  but  the  results 
have  not  been  encouraging.  A  risk  sufficient  in  itself  to 
prevent  resource  to  either  of  these  proceedings,  except  in  an 
absolutely  desperate  case,  is  the  possibility  of  a  clot  formed 
around  the  pole  of  a  galvanic  battery,  or  on  the  coils  of 
wire,  being  carried  into  the  carotid  or  vertebral  arteries, 
and  giving  rise  to  a  cerebral  embolism. 

Injections  of  a  solution  of  gelatine  into  the  buttock, 
with  a  view  to  increasing  the  coagulability  of  the  blood 
and  the  tendency  to  clotting  in  the  sac,  have  been  prac- 
tised,  but  the  good  results  claimed  in  some  cases  are  open 
to  suspicion,  and  fatal  cases  of  tetanus  from  imperfect 
sterilization  of  the  gelatine  employed  have  been  recorded, 
so  that  this  method  of  treatment  is  not  to  be  recommended. 
Increase  in  coagulability  of  the  blood  can  be  more  safely 
and  efficiently  effected  by  limitation  of  the  amount  of 
fluids,  and  by  the  administration  of  chloride  or  lactate  of 
calcium  in  doses  of  from  10  to  15  grains  two  or  three  times 
a  day.  A  milk  diet  may,  to  a  certain  extent,  contribute 
to  this  object,  as  milk  contains  a  considerable  proportion 
of  lime  salts.  It  is  also  beneficial  in  that  it  contains  no 
extractives  or  toxic  materials,  is  non-stimulating,  throws 
least  work  on  the  kidneys,  and  is  slightly  diuretic. 

Satisfactory  results  from  treatment  can  only  be  hoped 
for  if  the  aneurysm  is  saccular,  with  a  relatively  small 
neck  to  the  sac,  so  that  the  circulation  in  the  sac  is  slug- 
gish, and  a  chance  is  afforded  for  the  deposition  of  fibrin 
on  its  walls.  The  deposit  of  layers  of  laminated  clot  will 
afford  support  to  the  walls  of  the  aneurysm,  and  help  to 
prevent  its  further  extension,  and  will  also  tend  gradually 
to  exclude  the  blood  from  it  by  occluding  the  sac. 


INDEX. 


Adherent  pericardium,  45 

Age,  as  affecting  hypertrophy,  101 

, prognosis,  142, 194, 220, 223 

■ , treatment,  245 

Alcohol,  241,  249,  412 
Ansemia,  87,  164,  227,  242,  298 
Anatomical  relations  of  aorta,  431 

• of  heart,  2 

Aneurysm  of  ascending  aorta,  453 

,  classification  of,  448 

of  descending  aorta,  467 

,  dissecting,  415 

,  etiology  of,  425 

of  heart,  358 

from  infective  embolus,  78 

,  intra-pericardial,  448 

,  pathogeny  of,  428 

,  physical  signs  of,  434 

,  pressure,  effects  of,  443 

,  prognosis  in,  470 

,  pulse  in,  438 

of  transverse  part  of  arch,  458 

,  treatment  of,  472 

Angina  pectoris,  322,  348,  359,  449 

,  diagnosis  of,  371 

,  etiology  of,  364 

■ ,  prognosis  in,  373 

,  spurious,  372 

■ ,  treatment  of,  374 

vasomotoria,  366 

Aorta,  anatomical  relations  of,  431 

,  aneurysm  of,  424 

,  atheroma  of,  411 

,  rupture  of,  428 

Aortic  area,  sounds  over,  16 

incompetence,  123,  421 

,  blood  pressure  in,  22,  421 

,  from  degenerative  changes, 

137,  421 

,  etiology  of,  122,  136,  421 

,  physical  signs  in,  123 

,  symptoms  in,  140 

with  stenosis,  98,  145 

,  treatment  of,  146,  254 

Aortic  second  sound,  accentuation  of, 

95 


Aortic  second  sound  in  aneurysm,  437 
■    in    dilatation    of 

aorta,  137,  421 
Aortitis,  acute,  405,  413 
Apex  beat,  absence  of,  10 

,  displacements  of,  10 

,  murmurs  at,  14 

,  sounds  at,  13 

Apoplectiform  seizures,  350,  402 
Apoplexy,  pulmonary,  180 
Arterial  tension,  20 

.  high,  causes  of,  27 

■ ■ , ,  effects  of,  169,  272, 

278,367,  411,430 
,  ,   treatment  of,  171, 

305,  423 
Arterio-sclerosis,  28,  320,  411 
Atheroma  of  aorta,  411 

of  coronary  artery,  321 

Auricle,  left,  4 

, ,  in  mitral  incompetence, 

158 

, , stenosis,  176 

, ,  rupture  of  aneurysm  into, 

453 

,  right,  2 

, ,  rupture  of  aneurysm  into, 

453 
Auscultation,  13 


B 

Balfour,  87,  364 
Barlow,  62 

Baths,  brine,  236,  303 
Blood  pressure,  22 

,  estimation  of,  23 

Bradycardia,  351,  398 


C 

Caffein,  257 
Calcification  of  aorta,  413 

of  coronary  artery,  322 

of  valves,  82 

Capillary  pulsation,  122 


476 


INDEX. 


Cardiac  aneurysm,  358 

dilatation,  281 

duluess,  4 

hypertrophy,  272 

movements,  6 

muscle,  properties  of,  385 

Cheadle,  60,  62,  409 

Childhood,  rheumatism  in,  60 

Chorea,  31,  58,  168 

Claudication  intermittente,  370 

Climate,  239 

Cloudy  swelling,  328 

Clubbing  of  fingers,  210 

Compensation,  108,  228 

Congenital  malformations  of  heart, 

206 
Coeruleus  morbus,  211 
Cole,  59 

Convallaria,  257 
Coronary  arteries,  affections  of,  320 


D 


Danger,  relative,  of  valvular  lesions, 
215 

Death,  sudden,  216,  322,  338,  348, 
362,  403,  449,  470 

Diastole,  shortening  of,  14,  296 

Diastolic  shock,  435 

Diet  in  angina  pectoris,  376 

in  aneurysm,  472 

in  atheroma  of  aorta,  422 

in  bradycardia,  404 

in  valvular  disease,  249 

Digitalis,  256 

in  aortic  disease,  261 

in  mitral  incompetence,  262 

■ stenosis,  266 

Dilatation  of  aorta,  137,  421 

of  heart,  281 

in  pericarditis,  34 

,  etiology  of,  282 

of  left  ventricle  in  aortic  re- 
gurgitation, 134 

in  mitral  regurgi- 
tation, 159 

of  right  ventricle,  310 

in  pericarditis,  34 

Diuretin,  258 

Ductus  arteriosus,  patent,  210 


E 


Effusion,  pericardial,  30,  35 
Embolism,  71,78,  324 
Endarteritis,  322,  415,  417,  426 
Endocarditis,  acute,  56 
,  chronic,  82 


Endocarditis,     malignant     or     per- 
nicious,  67 
Epileptiform  attacks,  351,  402 
Erythema  marginatum,  63 

nodosum,  63 

Exercise,  233 

,  graduated,  235 

Exercises  resisted,  237 


F 


Fatty  degeneration  of  heart,  342 

infiltration  of  heart,  343 

Fibrosis  of  heart,  330 
First  sound,  modification  of,  13,  93, 
187 

in  mitral  stenosis,  183 

in  cardiac  dilatation,  294 

,  reduplication  of,  14,  95 

Fischer,  427,  429 
Foramen  ovale,  patent,  209 
Friction,  pericardial,  32 
Functional  affections  of  heart,  381 


G 


Gairdner,  174 
Gibson,  334,  346,  387 
Gout,  365,  372,  418 
Graves'  disease,  394 


II 


Etemic  murmurs,  112,  164 
Hpemoptysis  in  aneurysm,  455 

in  mitral  stenosis,  189 

Head,  382 

Heart,  aneurysm  of,  382 

,  examination  of,  7 

,  movements  of,  6 

,  muscle  properties  of,  385 

,  relations  of,  2 

sounds,  modification  of,  13,  93 

Heredity  as  affecting  prognosis,  224 

in  vascular   degeneration,   27, 

411 

High  arterial  tension.    Vide  Arterial 

Tension. 
Huchard,   322,    325,  330,   334,   346, 

368,  395,  404,  417,  427 
Hydropericardium,  52 
Hypera2inia  passive  of  lungs,  157 
Hypertonus,  arterial,  26.  439 
Hypertrophy  of  heart,  272 
,  etiology  of,  272 

in    aortic    incompetence, 

104,  135 


INDEX. 


477 


Hypertrophy     of    heart     in     aortic 

stenosis,  103,  116 
in   mitral   incompetence, 

107 
of  right  ventricle,  106,  273 


Impulse,  cardiac,  7 
Infarct,  pulmonary,  179 

of  kidney,  71,  77 

of  spleen,  71,  77 

Induration,  brown,  of  lung,  157 
Inspection,  examination  by,  7 
Intermittency  of  pulse,  3S7 
Irregularity  of  pulse,  389 

in  aortic  lesions,  136 

in  dilatation,  292 

in  mitral   incompetence, 

115 
Interstitial  myocarditis,  334 
Interventricular  septum  incomplete, 

207 


Janeway,  23 

Jugular  veins,  distension  of,  9,  201, 

202,  444 
,  pulsation  of,  9,  201,  230, 

300,  400,  401 


K 

Kidney,  infarct  of,  71,  77 


Lauder  Brunton,  370 

Laryngeal  nerve,  recurrent,  pressure 

on,  446,  459,  465 

,  relations  of,  433 

Leeches,  use  of,  43,  254,  304 

Lees,  35,  43,  451 

Liver,  enlargement  of,  11,  161,  189, 

201,  230,  252,  300 

,  nutmeg,  181 

,  pulsation  of,  12,  161,  189 


M 


McAlister,  164 

Mackenzie,  9,  202,  369,  382,  3S6,  400 
MacWilliam,  430 

Malformations  of  heart,  congenital, 
206 


Mitral  area,  sounds  over,  13 

incompetence,  151 

,  effects  on  heart  of,  106, 

259 

,  digitalis  in,  172,  262 

,  etiology  of,  S5,  151,  164, 

282 

,  pulse  in,  98,  154 

,  prognosis  in,  161 

,  symptoms  in,  161 

,  treatment  of,  170,  264 

stenosis,  174 

,  digitalis  iu,  199,  266 

,  effects  on  heart  of,  106, 

175 

,  etiology  of,  174 

,  morbid  anatomy,  175 

,  pulse  in,  98,  181 

,  prognosis  in,  193 

,  stages  of,  184 

,  symptoms  in,  189 

■ ,  treatment  of,  196,  266 

Morphia  in  angina  pectoris,  378 

in  aneurysm,  473 

in  aortic  regurgitation,  149 

in  pericarditis,  43 

Murmurs,  aortic  systolic,  111,  112 

■ ,  diastolic,  112,  421 

,  Flint  Austin,  125,  193 

,  bseniic.     Tide  under  Hsernic 

,  presystolic,  125,  183,  193 

,  pulmonic,  203,  208 

,  retarded  systolic,  157 

,  systolic,  mitral,  152,  295 

,  tricuspid,  200 

Myocarditis,  acute,  326 

■ ,  chronic,  330,  334 

Myocardium,  affections  of,  326,  sq. 

,  fatty  degeneration  of,  343 

,  fibrosis  of,  320 

,  syphilitic  disease  of,  336 


N 

Nauheini,  236,  303 
Nerves,  cardiac,  386 
Neuroses  of  heart,  381 
Nodules,  rheumatic,  39,  62 
"  Nutmeg  "  liver,  181 


O 


Occupation   as    affecting    prognosis, 

226 
CErtel  treatment,  235 
Osier,  399 


478 


INDEX. 


Pain  of  angina  pectoris,  360 

,  cardiac,  3S1 

, ,  causes  of,  383 

Paine,  32,  58 
Palpation,  9 
Palpitation,  390 
Paracentesis,  pericardii,  35,  44 
Paroxysmal  tachycardia,  394 
Peacock,  207 
Percussion,  12 
Pericardium,  adherent,  45 

,  new  growths  of,  55 

,  tuberculosis  of,  54 

Pericarditis,  acute,  30 

in  Bright's  disease,  44 

,  suppurative,  51 

Phillips,  217,  237 
Pneumopericardium,  53 
Poynton,  32,  35,  58,  409 
Pressure,  blood,  21 
Prognosis  in  aneurysm,  470 

in  angina  pectoris,  373 

in  aortic  incompetence,  141 

stenosis,  119 

in  dilatation,  300 

in  endocarditis,  acute,  63 

,  pernicious,  8L 

in  mitral  incompetence,  161 

stenosis,  193 

in  pericarditis,  42 

in  valvular  disease  (general),  214 

Powell,  Douglas,  346 

Pulmonary       artery,      rupture       of 

aneurysm  into,  450 
Pulmonic  area,  sounds  over,  16 

incompetence,  203 

stenosis,  203,  208 

second  sound,  accentuation  of, 

94,  184 
Pulse    in    aortic    incompetence,   96, 

127,  132 

stenosis,  96,  117 

incompetence  with  stenosis, 

130,  133,  145 

,  collapsing,  127 

,  Corrigan's,  127 

,  delay  of,  in  aneurysm,  441 

— : — ,  ,  in  aortic  incompetence, 

129 

in  mitral  incompetence,  97, 154 

stenosis,  97,  181 

,  intermittency  of,  387 

,  irregular,  389 

, ,  in  aortic  disease,  1 30 

, ,in  mitral  disease,  154, 182 

Pulsus  alternans,  369 

bisferiens,  130 

Pseudo-angina,  373 


R 


Retraction  of  intercostal   spaces,  8 

46 
Residence,  choice  of,  240 
Rosenfeld,  343 
Rupture  of  aneurysm,  450,  460 

of  aorta,  428 

of  heart,  348 

of  valve,  137 

Rhythm  of  heart,  disorders  of,  385 


S 


Schott  treatment,  236,  303 
Second  sound,  reduplication  of,  95 
Sensory  areas  cutaneous,  relation  of, 

to  visceral  affections,  382 
Serum,  antistreptococcic,  82 
Sex  as  affecting  prognosis,  224 
Sinus  of  valsalva,  448 
Sounds  of  heart,  13,  93 
Steven,  Lindsay,  333 
Spygmograph,  20 
Spygmomanometer,  23 
Spartein,  257 
Stomach,  dilatation  of,  318,  357,  392, 

404 
Strnphanthus,  257 
Stokes-Adams  disease,  399 
Syj)hilis  as  cause  of  aneurysm,  420 

— of  atheroma,  413,  415,  417 

of  chronic  endocarditis,  83 

of  myocardial  fibrosis,  336 


T 


Tachycardia,  393 
Tenderness,  praecardial,  382 
Thrill  in  aneurysm,  435,  450 

in  mitral  stenosis,  183 

Tracheal  tug,  436 
Treatment  in  aneurysm,  472 

in  angina  pectoris,  374 

in  aortic  incompetence,  146,  261 

stenosis,  121,  262 

in  atheroma,  422 

in  bradycardia,  404 

in  dilatation  of  heart,  303 

in  endocarditis,  acute,  65 

,  pernicious,  81 

in  fatty  degeneration,  355 

in  functional  affections  of  heart, 

384,  392 

in  mitral  incompetence,  170,  202 

stenosis,  196,  266 

in  pericarditis,  43 

,  GErtel,  235 


INDEX. 


479 


Treatment,  Scliott,  236,  303 

in  valvular  disease  (general), 

232 
Tricuspid  area,  15 

incompetence,  200 

stenosis,  202 


Valvular  lesions,  changes  in   heart 

in,  100 
.  estimation  of  extent  of, 

91 

,  etiology  of,  S4 

.  pulse  in,  96 


Valvular  lesions,  prognosis   general 

in,  214 

,  treatment  of,  232 

Vaso-rlilators,  uses  of,  122,  149,  199, 

254,  377,  422 
Venesection,  150,  252,  304,  473 
Vena  cava  superior,  pressure  on,  443, 

449 
,  rupture  of  aneuiysni 

into,  451 


W 

Walshe,  101 
Water-hammer  pulse,  127 


THE   END. 


PRINTED  BY    WILLIAM   CLOWES  AND  SONS,    LIMITED,    LONDON   AND    BECCLFS; 


I 


COLUMBIA  UNIVERSITY  LIBRARIES 


0037572547 


RC68S 

Broadbent 

Heart  disease  and  aneurysm  of  the 

aorta. 


